Materiały źródłowe

• #1 Pathophysiology of Hypertension: Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension

  https://emedicine.medscape.com/article/1937383-overview

  The pathogenesis of essential hypertension (primary hypertension, idiopathic hypertension) is multifactorial and highly complex, often involving reciprocal influences between different cardiovascular control systems. […] The kidney is both the contributing and the target organ of the hypertensive processes, and the disease involves the interaction of multiple organ systems and numerous mechanisms of independent or interdependent pathways. Factors that play an important role in the pathogenesis of hypertension include the aging process, genetics, activation of neurohormonal systems such as the sympathetic nervous system and renin-angiotensin-aldosterone system, obesity, gut microbiome, and increased dietary salt intake. […] The hallmark hemodynamic anomaly that is key to elevated blood pressure (BP) is an increase of systemic vascular resistance, caused by altered cardiovascular regulatory systems (such as through genetic and environmental factors).

• #1 Hypertension – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/hypertension/hypertension

  Increased CO […] Increased TPR […] Both […] In most patients with hypertension, CO is normal or slightly increased, and TPR is increased. This pattern is typical of primary hypertension and hypertension due to primary aldosteronism, pheochromocytoma, renovascular disease, and renal parenchymal disease. […] In many cases of hypertension, sodium transport across the vascular cell membrane is abnormal, because the sodium-potassium pump (Na+, K+-ATPase) is defective or inhibited, or because permeability to sodium ions is increased. The result is increased intracellular sodium and calcium, which makes the cell more sensitive to sympathetic stimulation. […] Sympathetic stimulation increases blood pressure, usually more in patients with hypertension than in patients who are normotensive.

• #2 The pathophysiology of hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC1120075/

  There is still much uncertainty about the pathophysiology of hypertension. A small number of patients (between 2% and 5%) have an underlying renal or adrenal disease as the cause for their raised blood pressure. In the remainder, however, no clear single identifiable cause is found and their condition is labelled essential hypertension. A number of physiological mechanisms are involved in the maintenance of normal blood pressure, and their derangement may play a part in the development of essential hypertension. […] It is probable that a great many interrelated factors contribute to the raised blood pressure in hypertensive patients, and their relative roles may differ between individuals. Among the factors that have been intensively studied are salt intake, obesity and insulin resistance, the renin-angiotensin system, and the sympathetic nervous system. In the past few years, other factors have been evaluated, including genetics, endothelial dysfunction (as manifested by changes in endothelin and nitric oxide), low birth weight and intrauterine nutrition, and neurovascular anomalies.

• #2 Advances in pathogenesis and treatment of essential hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9616110/

  Hypertension is a significant risk factor for cardiovascular and cerebrovascular diseases and the leading cause of premature death worldwide. However, the pathogenesis of the hypertension, especially essential hypertension, is complex and requires in-depth studies. Recently, new findings about essential hypertension have emerged, and these may provide important theoretical bases and therapeutic tools to break through the existing bottleneck of essential hypertension. […] Essential hypertension accounts for more than 90% of all hypertensive patients, but the exact underlying mechanisms remain ambiguous. […] Therefore, the investigation of the causative mechanism has been the key research direction of essential hypertension. There are two factors that affect BP directly, including vasodilation capacity and the volume of intravascular fluid.

• #2 The pathophysiology of hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC1120075/

  Maintenance of a normal blood pressure is dependent on the balance between the cardiac output and peripheral vascular resistance. Most patients with essential hypertension have a normal cardiac output but a raised peripheral resistance. Peripheral resistance is determined not by large arteries or the capillaries but by small arterioles, the walls of which contain smooth muscle cells. Contraction of smooth muscle cells is thought to be related to a rise in intracellular calcium concentration, which may explain the vasodilatory effect of drugs that block the calcium channels. Prolonged smooth muscle constriction is thought to induce structural changes with thickening of the arteriolar vessel walls possibly mediated by angiotensin, leading to an irreversible rise in peripheral resistance. […] The renin-angiotensin system may be the most important of the endocrine systems that affect the control of blood pressure. Renin is secreted from the juxtaglomerular apparatus of the kidney in response to glomerular underperfusion or a reduced salt intake. It is also released in response to stimulation from the sympathetic nervous system.

• #3 Pathophysiology of Hypertension: Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension

  https://emedicine.medscape.com/article/1937383-overview

  The pathogenesis of essential hypertension (primary hypertension, idiopathic hypertension) is multifactorial and highly complex, often involving reciprocal influences between different cardiovascular control systems. […] The kidney is both the contributing and the target organ of the hypertensive processes, and the disease involves the interaction of multiple organ systems and numerous mechanisms of independent or interdependent pathways. Factors that play an important role in the pathogenesis of hypertension include the aging process, genetics, activation of neurohormonal systems such as the sympathetic nervous system and renin-angiotensin-aldosterone system, obesity, gut microbiome, and increased dietary salt intake. […] The hallmark hemodynamic anomaly that is key to elevated blood pressure (BP) is an increase of systemic vascular resistance, caused by altered cardiovascular regulatory systems (such as through genetic and environmental factors).

• #3 The pathophysiology of hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC1120075/

  There is still much uncertainty about the pathophysiology of hypertension. A small number of patients (between 2% and 5%) have an underlying renal or adrenal disease as the cause for their raised blood pressure. In the remainder, however, no clear single identifiable cause is found and their condition is labelled essential hypertension. A number of physiological mechanisms are involved in the maintenance of normal blood pressure, and their derangement may play a part in the development of essential hypertension. […] It is probable that a great many interrelated factors contribute to the raised blood pressure in hypertensive patients, and their relative roles may differ between individuals. Among the factors that have been intensively studied are salt intake, obesity and insulin resistance, the renin-angiotensin system, and the sympathetic nervous system. In the past few years, other factors have been evaluated, including genetics, endothelial dysfunction (as manifested by changes in endothelin and nitric oxide), low birth weight and intrauterine nutrition, and neurovascular anomalies.

• #3 Pathophysiology of Hypertension: Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension

  https://emedicine.medscape.com/article/1937383-overview

  The progression of essential hypertension begins with prehypertension in persons aged 10-30 years (by increased cardiac output); then advances to early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent); then progresses to established hypertension in persons aged 30-50 years; and finally advances to complicated hypertension in persons aged 40-60 years. […] Patients who develop hypertension are known to develop a systemic hypertensive response secondary to vasoconstrictive stimuli. Alterations in structural and physical properties of resistance arteries, as well as changes in endothelial function, are probably responsible for this abnormal behavior of the vasculature. […] Furthermore, vascular remodeling occurs over the years as hypertension evolves, thereby maintaining increased vascular resistance irrespective of the initial hemodynamic pattern.

• #4 Pathophysiology of Hypertension: Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension

  https://emedicine.medscape.com/article/1937383-overview

  The pathogenesis of essential hypertension (primary hypertension, idiopathic hypertension) is multifactorial and highly complex, often involving reciprocal influences between different cardiovascular control systems. […] The kidney is both the contributing and the target organ of the hypertensive processes, and the disease involves the interaction of multiple organ systems and numerous mechanisms of independent or interdependent pathways. Factors that play an important role in the pathogenesis of hypertension include the aging process, genetics, activation of neurohormonal systems such as the sympathetic nervous system and renin-angiotensin-aldosterone system, obesity, gut microbiome, and increased dietary salt intake. […] The hallmark hemodynamic anomaly that is key to elevated blood pressure (BP) is an increase of systemic vascular resistance, caused by altered cardiovascular regulatory systems (such as through genetic and environmental factors).

• #4 Pathophysiology of Hypertension: Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension

  https://emedicine.medscape.com/article/1937383-overview

  Changes in vascular wall thickness affect the amplification of peripheral vascular resistance in hypertensive patients and result in the reflection of waves back to the aorta, increasing systolic BP. […] One form of essential hypertension, termed high-output hypertension, results from decreased peripheral vascular resistance and concomitant cardiac stimulation by adrenergic hyperactivity and altered calcium homeostasis. A second mechanism manifests with normal or reduced cardiac output and elevated systemic vascular resistance (SVR) due to increased vasoreactivity. […] Another (and overlapping) mechanism is increased salt and water reabsorption (salt sensitivity) by the kidney, which increases circulating blood volume. […] Finally, an inflammatory process often accompanies hypertension. Activated immune cells infiltrate and alter the function and structure of various organs, including the vasculature and the kidney. The inflammatory process is not thought to cause hypertension on its own, but rather to intensify dysfunction of the kidney and the vasculature. That is, it promotes BP elevation as well as the end-organ damage associated with hypertension.

• #5 The pathophysiology of hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC1120075/

  There is still much uncertainty about the pathophysiology of hypertension. A small number of patients (between 2% and 5%) have an underlying renal or adrenal disease as the cause for their raised blood pressure. In the remainder, however, no clear single identifiable cause is found and their condition is labelled essential hypertension. A number of physiological mechanisms are involved in the maintenance of normal blood pressure, and their derangement may play a part in the development of essential hypertension. […] It is probable that a great many interrelated factors contribute to the raised blood pressure in hypertensive patients, and their relative roles may differ between individuals. Among the factors that have been intensively studied are salt intake, obesity and insulin resistance, the renin-angiotensin system, and the sympathetic nervous system. In the past few years, other factors have been evaluated, including genetics, endothelial dysfunction (as manifested by changes in endothelin and nitric oxide), low birth weight and intrauterine nutrition, and neurovascular anomalies.

• #5 Salt and hypertension: current views

  https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-22/salt-and-hypertension-current-views

  When the sodium excretory ability of the kidney is compromised, hypertension may develop. […] Increase in systemic peripheral resistance as high sodium triggers remodelling in small resistant arteries – The effect of sodium on the vascular remodelling of small resistant arteries can occur both in normotensive as well as in hypertensive individuals. […] Endothelial dysfunction – it was found that high salt intake can cause marked reduction in the endothelial nitric oxide (NO) which is responsible for endothelium-dependent vascular dilatation. […] Reduction of NO leads to not only elevation of blood pressure, but also to many blood pressure-independent cardiovascular complications. […] Changes in the structure and function of large elastic arteries – it was found that high salt intake could affect the properties of large elastic arteries leading to an increase in vascular stiffness.

• #6 Pathophysiology of Hypertension: Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension

  https://emedicine.medscape.com/article/1937383-overview

  The progression of essential hypertension begins with prehypertension in persons aged 10-30 years (by increased cardiac output); then advances to early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent); then progresses to established hypertension in persons aged 30-50 years; and finally advances to complicated hypertension in persons aged 40-60 years. […] Patients who develop hypertension are known to develop a systemic hypertensive response secondary to vasoconstrictive stimuli. Alterations in structural and physical properties of resistance arteries, as well as changes in endothelial function, are probably responsible for this abnormal behavior of the vasculature. […] Furthermore, vascular remodeling occurs over the years as hypertension evolves, thereby maintaining increased vascular resistance irrespective of the initial hemodynamic pattern.

• #7 Pathophysiology of Hypertension: Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension

  https://emedicine.medscape.com/article/1937383-overview

  Changes in vascular wall thickness affect the amplification of peripheral vascular resistance in hypertensive patients and result in the reflection of waves back to the aorta, increasing systolic BP. […] One form of essential hypertension, termed high-output hypertension, results from decreased peripheral vascular resistance and concomitant cardiac stimulation by adrenergic hyperactivity and altered calcium homeostasis. A second mechanism manifests with normal or reduced cardiac output and elevated systemic vascular resistance (SVR) due to increased vasoreactivity. […] Another (and overlapping) mechanism is increased salt and water reabsorption (salt sensitivity) by the kidney, which increases circulating blood volume. […] Finally, an inflammatory process often accompanies hypertension. Activated immune cells infiltrate and alter the function and structure of various organs, including the vasculature and the kidney. The inflammatory process is not thought to cause hypertension on its own, but rather to intensify dysfunction of the kidney and the vasculature. That is, it promotes BP elevation as well as the end-organ damage associated with hypertension.

• #8 The pathophysiology of hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC1120075/

  Maintenance of a normal blood pressure is dependent on the balance between the cardiac output and peripheral vascular resistance. Most patients with essential hypertension have a normal cardiac output but a raised peripheral resistance. Peripheral resistance is determined not by large arteries or the capillaries but by small arterioles, the walls of which contain smooth muscle cells. Contraction of smooth muscle cells is thought to be related to a rise in intracellular calcium concentration, which may explain the vasodilatory effect of drugs that block the calcium channels. Prolonged smooth muscle constriction is thought to induce structural changes with thickening of the arteriolar vessel walls possibly mediated by angiotensin, leading to an irreversible rise in peripheral resistance. […] The renin-angiotensin system may be the most important of the endocrine systems that affect the control of blood pressure. Renin is secreted from the juxtaglomerular apparatus of the kidney in response to glomerular underperfusion or a reduced salt intake. It is also released in response to stimulation from the sympathetic nervous system.

• #9 Pathophysiology of hypertension – Wikipedia

  https://en.wikipedia.org/wiki/Pathophysiology_of_hypertension

  Resistant hypertension can be treated by electrically stimulating the baroreflex with a pacemaker-like device. […] Another system maintaining the extracellular fluid volume, peripheral resistance, and that if disturbed may lead to hypertension, is the renin-angiotensin-aldosterone system. Renin is a circulating enzyme that participates in maintaining extracellular volume and arterial vasoconstriction, therefore contributing to regulation of blood pressure. It performs this function by breaking down (hydrolysing) angiotensinogen, secreted from the liver, into the peptide angiotensin I. Angiotensin I is further cleaved by an enzyme that is located primarily but not exclusively in the pulmonary circulation bound to endothelium; that enzyme is angiotensin converting enzyme (ACE). This cleavage produces angiotensin II, the most vasoactive peptide. Angiotensin II is a potent constrictor of all blood vessels. It acts on the musculature of arteries, raising peripheral resistance and thereby elevating blood pressure. Angiotensin II also causes the adrenal glands to release aldosterone, which stimulates the epithelial cells of the kidneys to increase re-absorption of salt and water, leading to raised blood volume and raised blood pressure. So elevated renin levels in the blood leads to hypertension.

• #10 The pathophysiology of hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC1120075/

  Maintenance of a normal blood pressure is dependent on the balance between the cardiac output and peripheral vascular resistance. Most patients with essential hypertension have a normal cardiac output but a raised peripheral resistance. Peripheral resistance is determined not by large arteries or the capillaries but by small arterioles, the walls of which contain smooth muscle cells. Contraction of smooth muscle cells is thought to be related to a rise in intracellular calcium concentration, which may explain the vasodilatory effect of drugs that block the calcium channels. Prolonged smooth muscle constriction is thought to induce structural changes with thickening of the arteriolar vessel walls possibly mediated by angiotensin, leading to an irreversible rise in peripheral resistance. […] The renin-angiotensin system may be the most important of the endocrine systems that affect the control of blood pressure. Renin is secreted from the juxtaglomerular apparatus of the kidney in response to glomerular underperfusion or a reduced salt intake. It is also released in response to stimulation from the sympathetic nervous system.

• #11 Pathophysiology of hypertension – Wikipedia

  https://en.wikipedia.org/wiki/Pathophysiology_of_hypertension

  Resistant hypertension can be treated by electrically stimulating the baroreflex with a pacemaker-like device. […] Another system maintaining the extracellular fluid volume, peripheral resistance, and that if disturbed may lead to hypertension, is the renin-angiotensin-aldosterone system. Renin is a circulating enzyme that participates in maintaining extracellular volume and arterial vasoconstriction, therefore contributing to regulation of blood pressure. It performs this function by breaking down (hydrolysing) angiotensinogen, secreted from the liver, into the peptide angiotensin I. Angiotensin I is further cleaved by an enzyme that is located primarily but not exclusively in the pulmonary circulation bound to endothelium; that enzyme is angiotensin converting enzyme (ACE). This cleavage produces angiotensin II, the most vasoactive peptide. Angiotensin II is a potent constrictor of all blood vessels. It acts on the musculature of arteries, raising peripheral resistance and thereby elevating blood pressure. Angiotensin II also causes the adrenal glands to release aldosterone, which stimulates the epithelial cells of the kidneys to increase re-absorption of salt and water, leading to raised blood volume and raised blood pressure. So elevated renin levels in the blood leads to hypertension.

• #12 Advances in pathogenesis and treatment of essential hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9616110/

  Water-sodium retention is a key cause of abnormal increases in intravascular fluid volume. […] High-salt intake is an important trigger in essential hypertension caused by water-sodium retention. […] Multiple factors may contribute to the development of salt-sensitive hypertension, including age, obesity, genetic background, and maternal conditions during fetal life etc., but the underlying mechanisms of salt-sensitive hypertension are not fully understood. […] Renin-angiotensin-aldosterone system regulates BP mainly by affecting arterial constriction and water-sodium retention in the body. […] Several components of axis cascade have been identified in the RAAS, including angiotensinogen, renin, angiotensin-converting enzyme, angiotensins with various subtypes, aldosterone and aldosterone receptors.

• #13 Advances in pathogenesis and treatment of essential hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9616110/

  Water-sodium retention is a key cause of abnormal increases in intravascular fluid volume. […] High-salt intake is an important trigger in essential hypertension caused by water-sodium retention. […] Multiple factors may contribute to the development of salt-sensitive hypertension, including age, obesity, genetic background, and maternal conditions during fetal life etc., but the underlying mechanisms of salt-sensitive hypertension are not fully understood. […] Renin-angiotensin-aldosterone system regulates BP mainly by affecting arterial constriction and water-sodium retention in the body. […] Several components of axis cascade have been identified in the RAAS, including angiotensinogen, renin, angiotensin-converting enzyme, angiotensins with various subtypes, aldosterone and aldosterone receptors.

• #14 Pathophysiology of hypertension – Wikipedia

  https://en.wikipedia.org/wiki/Pathophysiology_of_hypertension

  Resistant hypertension can be treated by electrically stimulating the baroreflex with a pacemaker-like device. […] Another system maintaining the extracellular fluid volume, peripheral resistance, and that if disturbed may lead to hypertension, is the renin-angiotensin-aldosterone system. Renin is a circulating enzyme that participates in maintaining extracellular volume and arterial vasoconstriction, therefore contributing to regulation of blood pressure. It performs this function by breaking down (hydrolysing) angiotensinogen, secreted from the liver, into the peptide angiotensin I. Angiotensin I is further cleaved by an enzyme that is located primarily but not exclusively in the pulmonary circulation bound to endothelium; that enzyme is angiotensin converting enzyme (ACE). This cleavage produces angiotensin II, the most vasoactive peptide. Angiotensin II is a potent constrictor of all blood vessels. It acts on the musculature of arteries, raising peripheral resistance and thereby elevating blood pressure. Angiotensin II also causes the adrenal glands to release aldosterone, which stimulates the epithelial cells of the kidneys to increase re-absorption of salt and water, leading to raised blood volume and raised blood pressure. So elevated renin levels in the blood leads to hypertension.

• #15 The pathophysiology of hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC1120075/

  The circulating renin-angiotensin system is not thought to be directly responsible for the rise in blood pressure in essential hypertension. In particular, many hypertensive patients have low levels of renin and angiotensin II (especially elderly and black people), and drugs that block the renin-angiotensin system are not particularly effective. […] There is, however, increasing evidence that there are important non-circulating local renin-angiotensin epicrine or paracrine systems, which also control blood pressure. Local renin systems have been reported in the kidney, the heart, and the arterial tree. They may have important roles in regulating regional blood flow. […] Sympathetic nervous system stimulation can cause both arteriolar constriction and arteriolar dilatation. Thus the autonomic nervous system has an important role in maintaining a normal blood pressure. It is also important in the mediation of short term changes in blood pressure in response to stress and physical exercise.

• #16 Pathophysiology of hypertension – Wikipedia

  https://en.wikipedia.org/wiki/Pathophysiology_of_hypertension

  Cardiac output and peripheral resistance are the two determinants of arterial pressure. Cardiac output is determined by stroke volume and heart rate; stroke volume is related to myocardial contractility and to the size of the vascular compartment. Peripheral resistance is determined by functional and anatomic changes in small arteries and arterioles. […] The autonomic nervous system plays a central role in maintaining cardiovascular homeostasis via pressure, volume, and chemoreceptor signals. It does this by regulating the peripheral vasculature, and kidney function, which in turn affect cardiac output, vascular resistance, and fluid retention. Excess activity of the sympathetic nervous system increases blood pressure and contributes to hypertension. The mechanisms of increased sympathetic nervous system activity in hypertension involve alterations in baroreflex and chemoreflex pathways at both peripheral and central levels. Arterial baroreceptors are reset to a higher pressure in hypertensive patients, and this peripheral resetting reverts to normal when arterial pressure is normalized. Furthermore, there is central resetting of the aortic baroreflex in hypertensive patients, resulting in suppression of sympathetic inhibition after activation of aortic baroreceptor nerves. This baroreflex resetting seems to be mediated, at least partly, by a central action of angiotensin II. Additional small-molecule mediators that suppress baroreceptor activity and contribute to exaggerated sympathetic drive in hypertension include reactive oxygen species and endothelin. Some studies have shown that hypertensive patients manifest greater vasoconstrictor responses to infused norepinephrine than normotensive controls. And that hypertensive patients do not show the normal response to increased circulating norepinephrine levels which generally induces downregulation of noradrenergic receptor, and it is believed that this abnormal response is genetically inherited.

• #17 Advances in pathogenesis and treatment of essential hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9616110/

  Sympathetic dysregulation is also an important cause of essential hypertension. […] The sympathetic overdrive leads to increased cardiac output, increased systemic vascular tone, and elevated plasma catecholamine levels. […] The interplay of these factors leads to a net-like pathogenesis of essential hypertension and increases the difficulty of the treatment. […] In our opinion, the pathogenesis of hypertension is based on both decreased vasodilation and increased blood volume.

• #18 Pathophysiology of hypertension – Wikipedia

  https://en.wikipedia.org/wiki/Pathophysiology_of_hypertension

  Cardiac output and peripheral resistance are the two determinants of arterial pressure. Cardiac output is determined by stroke volume and heart rate; stroke volume is related to myocardial contractility and to the size of the vascular compartment. Peripheral resistance is determined by functional and anatomic changes in small arteries and arterioles. […] The autonomic nervous system plays a central role in maintaining cardiovascular homeostasis via pressure, volume, and chemoreceptor signals. It does this by regulating the peripheral vasculature, and kidney function, which in turn affect cardiac output, vascular resistance, and fluid retention. Excess activity of the sympathetic nervous system increases blood pressure and contributes to hypertension. The mechanisms of increased sympathetic nervous system activity in hypertension involve alterations in baroreflex and chemoreflex pathways at both peripheral and central levels. Arterial baroreceptors are reset to a higher pressure in hypertensive patients, and this peripheral resetting reverts to normal when arterial pressure is normalized. Furthermore, there is central resetting of the aortic baroreflex in hypertensive patients, resulting in suppression of sympathetic inhibition after activation of aortic baroreceptor nerves. This baroreflex resetting seems to be mediated, at least partly, by a central action of angiotensin II. Additional small-molecule mediators that suppress baroreceptor activity and contribute to exaggerated sympathetic drive in hypertension include reactive oxygen species and endothelin. Some studies have shown that hypertensive patients manifest greater vasoconstrictor responses to infused norepinephrine than normotensive controls. And that hypertensive patients do not show the normal response to increased circulating norepinephrine levels which generally induces downregulation of noradrenergic receptor, and it is believed that this abnormal response is genetically inherited.

• #19 Pathophysiology of hypertension – Wikipedia

  https://en.wikipedia.org/wiki/Pathophysiology_of_hypertension

  Cardiac output and peripheral resistance are the two determinants of arterial pressure. Cardiac output is determined by stroke volume and heart rate; stroke volume is related to myocardial contractility and to the size of the vascular compartment. Peripheral resistance is determined by functional and anatomic changes in small arteries and arterioles. […] The autonomic nervous system plays a central role in maintaining cardiovascular homeostasis via pressure, volume, and chemoreceptor signals. It does this by regulating the peripheral vasculature, and kidney function, which in turn affect cardiac output, vascular resistance, and fluid retention. Excess activity of the sympathetic nervous system increases blood pressure and contributes to hypertension. The mechanisms of increased sympathetic nervous system activity in hypertension involve alterations in baroreflex and chemoreflex pathways at both peripheral and central levels. Arterial baroreceptors are reset to a higher pressure in hypertensive patients, and this peripheral resetting reverts to normal when arterial pressure is normalized. Furthermore, there is central resetting of the aortic baroreflex in hypertensive patients, resulting in suppression of sympathetic inhibition after activation of aortic baroreceptor nerves. This baroreflex resetting seems to be mediated, at least partly, by a central action of angiotensin II. Additional small-molecule mediators that suppress baroreceptor activity and contribute to exaggerated sympathetic drive in hypertension include reactive oxygen species and endothelin. Some studies have shown that hypertensive patients manifest greater vasoconstrictor responses to infused norepinephrine than normotensive controls. And that hypertensive patients do not show the normal response to increased circulating norepinephrine levels which generally induces downregulation of noradrenergic receptor, and it is believed that this abnormal response is genetically inherited.

• #20 Pathophysiology of hypertension – Wikipedia

  https://en.wikipedia.org/wiki/Pathophysiology_of_hypertension

  Cardiac output and peripheral resistance are the two determinants of arterial pressure. Cardiac output is determined by stroke volume and heart rate; stroke volume is related to myocardial contractility and to the size of the vascular compartment. Peripheral resistance is determined by functional and anatomic changes in small arteries and arterioles. […] The autonomic nervous system plays a central role in maintaining cardiovascular homeostasis via pressure, volume, and chemoreceptor signals. It does this by regulating the peripheral vasculature, and kidney function, which in turn affect cardiac output, vascular resistance, and fluid retention. Excess activity of the sympathetic nervous system increases blood pressure and contributes to hypertension. The mechanisms of increased sympathetic nervous system activity in hypertension involve alterations in baroreflex and chemoreflex pathways at both peripheral and central levels. Arterial baroreceptors are reset to a higher pressure in hypertensive patients, and this peripheral resetting reverts to normal when arterial pressure is normalized. Furthermore, there is central resetting of the aortic baroreflex in hypertensive patients, resulting in suppression of sympathetic inhibition after activation of aortic baroreceptor nerves. This baroreflex resetting seems to be mediated, at least partly, by a central action of angiotensin II. Additional small-molecule mediators that suppress baroreceptor activity and contribute to exaggerated sympathetic drive in hypertension include reactive oxygen species and endothelin. Some studies have shown that hypertensive patients manifest greater vasoconstrictor responses to infused norepinephrine than normotensive controls. And that hypertensive patients do not show the normal response to increased circulating norepinephrine levels which generally induces downregulation of noradrenergic receptor, and it is believed that this abnormal response is genetically inherited.

• #21 Advances in pathogenesis and treatment of essential hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9616110/

  Sympathetic dysregulation is also an important cause of essential hypertension. […] The sympathetic overdrive leads to increased cardiac output, increased systemic vascular tone, and elevated plasma catecholamine levels. […] The interplay of these factors leads to a net-like pathogenesis of essential hypertension and increases the difficulty of the treatment. […] In our opinion, the pathogenesis of hypertension is based on both decreased vasodilation and increased blood volume.

• #22 Signaling pathways in vascular function and hypertension: molecular mechanisms and therapeutic interventions | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-023-01430-7

  The NO-NOsGC-cGMP pathway is closely linked to the contractile function of VSMCs, and its activation precedes the development of hypertension. […] Vascular remodeling presents as vascular lumen narrowing, vascular wall thickening, and elasticity loss. […] Abnormal vascular structure is an important cause of hypertension and cardiovascular events. […] The changes of ECM mainly occur in the media, which may be related to the different SMC phenotypes and different secretory factors from SMCs. […] The renin-angiotensin-aldosterone system (RAAS) plays a critical role in the regulation of BP. […] The signaling pathways of RAAS in cells begin with the activation of various receptors, and the diverse effects of RAAS can be attributed to the activation of different receptors. […] The innate immunity serves as the initial defense against infectious agents and also contributes significantly to the development of sterile inflammation. […] The activation of muscle sympathetic nerve activity (SNA) is the key mechanism of sympathetic dysregulation leading to hypertension.

• #23 Advances in pathogenesis and treatment of essential hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9616110/

  Water-sodium retention is a key cause of abnormal increases in intravascular fluid volume. […] High-salt intake is an important trigger in essential hypertension caused by water-sodium retention. […] Multiple factors may contribute to the development of salt-sensitive hypertension, including age, obesity, genetic background, and maternal conditions during fetal life etc., but the underlying mechanisms of salt-sensitive hypertension are not fully understood. […] Renin-angiotensin-aldosterone system regulates BP mainly by affecting arterial constriction and water-sodium retention in the body. […] Several components of axis cascade have been identified in the RAAS, including angiotensinogen, renin, angiotensin-converting enzyme, angiotensins with various subtypes, aldosterone and aldosterone receptors.

• #24 Advances in pathogenesis and treatment of essential hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9616110/

  Water-sodium retention is a key cause of abnormal increases in intravascular fluid volume. […] High-salt intake is an important trigger in essential hypertension caused by water-sodium retention. […] Multiple factors may contribute to the development of salt-sensitive hypertension, including age, obesity, genetic background, and maternal conditions during fetal life etc., but the underlying mechanisms of salt-sensitive hypertension are not fully understood. […] Renin-angiotensin-aldosterone system regulates BP mainly by affecting arterial constriction and water-sodium retention in the body. […] Several components of axis cascade have been identified in the RAAS, including angiotensinogen, renin, angiotensin-converting enzyme, angiotensins with various subtypes, aldosterone and aldosterone receptors.

• #25 Salt and hypertension: current views

  https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-22/salt-and-hypertension-current-views

  Excessive intake of sodium (defined by the World Health Organization [WHO] as more than 2 g of sodium or more than 5 g of sodium chloride per day) is directly linked to high blood pressure and it was found that the higher the daily salt intake, the higher the systolic blood pressure. […] In addition, high salt intake was found to blunt the physiologic nocturnal blood pressure dipping and to increase the daytime heart rate in ambulatory blood pressure monitoring. […] There are many mechanisms that link high salt intake and hypertension: Water retention – this was explained by the classic concept of Guyton, who demonstrated that high salt intake leads to more water retention, which leads to an expansion in the circulating volumes, an increase in cardiac output, and a rise in kidney perfusion pressure.

• #26 Salt and hypertension: current views

  https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-22/salt-and-hypertension-current-views

  When the sodium excretory ability of the kidney is compromised, hypertension may develop. […] Increase in systemic peripheral resistance as high sodium triggers remodelling in small resistant arteries – The effect of sodium on the vascular remodelling of small resistant arteries can occur both in normotensive as well as in hypertensive individuals. […] Endothelial dysfunction – it was found that high salt intake can cause marked reduction in the endothelial nitric oxide (NO) which is responsible for endothelium-dependent vascular dilatation. […] Reduction of NO leads to not only elevation of blood pressure, but also to many blood pressure-independent cardiovascular complications. […] Changes in the structure and function of large elastic arteries – it was found that high salt intake could affect the properties of large elastic arteries leading to an increase in vascular stiffness.

• #27 Salt and hypertension: current views

  https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-22/salt-and-hypertension-current-views

  When the sodium excretory ability of the kidney is compromised, hypertension may develop. […] Increase in systemic peripheral resistance as high sodium triggers remodelling in small resistant arteries – The effect of sodium on the vascular remodelling of small resistant arteries can occur both in normotensive as well as in hypertensive individuals. […] Endothelial dysfunction – it was found that high salt intake can cause marked reduction in the endothelial nitric oxide (NO) which is responsible for endothelium-dependent vascular dilatation. […] Reduction of NO leads to not only elevation of blood pressure, but also to many blood pressure-independent cardiovascular complications. […] Changes in the structure and function of large elastic arteries – it was found that high salt intake could affect the properties of large elastic arteries leading to an increase in vascular stiffness.

• #28 Salt and hypertension: current views

  https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-22/salt-and-hypertension-current-views

  Modulation in the autonomic neuronal supply and the sympathetic activity of the cardiovascular system. […] Salt sensitivity is defined as the individuals blood pressure susceptibility to dietary salt intake where changes in blood pressure parallel changes in salt consumption. […] In salt-sensitive individuals, the physiologic pressure-natriuresis mechanism is impaired and the kidney becomes unable to excrete a sufficient amount of sodium in response to a high sodium intake. […] Despite the clear association between salt sensitivity and pathophysiological mechanisms of hypertension, physicians cannot not use this fact in everyday clinical practice, simply because of the lack of a practical diagnostic test for salt sensitivity. […] It has been shown that salt restriction can lower blood pressure, where a reduction of about 1.75 g sodium per day (4.4 g sodium chloride/day) was associated with a mean reduction in systolic/diastolic blood pressure of 4.2/2.1 mmHg, respectively.

• #29 The pathophysiology of hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC1120075/

  It is probable that hypertension is related to an interaction between the autonomic nervous system and the renin-angiotensin system, together with other factors, including sodium, circulating volume, and some of the more recently described hormones. […] Dysfunction of the endothelium has been implicated in human essential hypertension. […] Modulation of endothelial function is an attractive therapeutic option in attempting to minimise some of the important complications of hypertension. […] Many other vasoactive systems and mechanisms affecting sodium transport and vascular tone are involved in the maintenance of a normal blood pressure. […] Patients with hypertension demonstrate abnormalities of vessel wall (endothelial dysfunction or damage), the blood constituents (abnormal levels of haemostatic factors, platelet activation, and fibrinolysis), and blood flow (rheology, viscosity, and flow reserve), suggesting that hypertension confers a prothrombotic or hypercoagulable state.

• #30 Hypertension | PPT

  https://www.slideshare.net/slideshow/hypertension-66802042/66802042

  The vascular endothelium is a single cell layer that lines the blood vessel. It will produce vasoactive substances and growth factors like nitric acid, endothelin etc.. These substances are potent vasoconstrictors and causes increases blood pressure level […] When the angiotensin-II is stimulated in the adrenal cortex, it will secrete aldosterone. The aldosterone will stimulate the kidneys to retain sodium and water. Thus the BP and cardiac output will get increased. […] Hypertension is defined as elevated blood pressure above 140/90 mmHg and can be essential or secondary. Common types include essential, secondary, white coat, and isolated systolic hypertension. […] The document discusses hypertension, including its definition, classification, epidemiology, types, etiology, pathophysiology, clinical presentation, diagnosis, and management. Hypertension is defined as elevated blood pressure above 140/90 mmHg and can be essential or secondary. Common types include essential, secondary, white coat, and isolated systolic hypertension. […] The pathophysiology involves the sympathetic nervous system, vascular endothelium, renal system, and endocrine system which regulate blood pressure.

• #31 The pathophysiology of hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC1120075/

  It is probable that hypertension is related to an interaction between the autonomic nervous system and the renin-angiotensin system, together with other factors, including sodium, circulating volume, and some of the more recently described hormones. […] Dysfunction of the endothelium has been implicated in human essential hypertension. […] Modulation of endothelial function is an attractive therapeutic option in attempting to minimise some of the important complications of hypertension. […] Many other vasoactive systems and mechanisms affecting sodium transport and vascular tone are involved in the maintenance of a normal blood pressure. […] Patients with hypertension demonstrate abnormalities of vessel wall (endothelial dysfunction or damage), the blood constituents (abnormal levels of haemostatic factors, platelet activation, and fibrinolysis), and blood flow (rheology, viscosity, and flow reserve), suggesting that hypertension confers a prothrombotic or hypercoagulable state.

• #32 Signaling pathways in vascular function and hypertension: molecular mechanisms and therapeutic interventions | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-023-01430-7

  Hypertension is a global public health issue and the leading cause of premature death in humans. […] The alterations in signaling pathways in these cells are the key molecular mechanisms underlying vascular dysfunction and hypertension development. […] Changes in signaling pathways in vascular endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) are key molecular mechanisms which trigger vascular dysfunction and promote the development of hypertension. […] The signaling pathways underlying vascular function and hypertension are complex. There are three classical ways to regulate vascular function and BP levels, including calcium signaling pathway, the NO (nitric oxide)-NOsGC (nitric oxide-sensitive guanylate cyclase)-cGMP pathway, and vascular remodeling. […] The primary mechanisms regulating the contractile state of VSMCs are changes in cytosolic calcium concentration ([Ca2+]c).

• #33 The pathophysiology of hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC1120075/

  It is probable that hypertension is related to an interaction between the autonomic nervous system and the renin-angiotensin system, together with other factors, including sodium, circulating volume, and some of the more recently described hormones. […] Dysfunction of the endothelium has been implicated in human essential hypertension. […] Modulation of endothelial function is an attractive therapeutic option in attempting to minimise some of the important complications of hypertension. […] Many other vasoactive systems and mechanisms affecting sodium transport and vascular tone are involved in the maintenance of a normal blood pressure. […] Patients with hypertension demonstrate abnormalities of vessel wall (endothelial dysfunction or damage), the blood constituents (abnormal levels of haemostatic factors, platelet activation, and fibrinolysis), and blood flow (rheology, viscosity, and flow reserve), suggesting that hypertension confers a prothrombotic or hypercoagulable state.

• #34 Pathophysiology of Hypertension: Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension

  https://emedicine.medscape.com/article/1937383-overview

  The progression of essential hypertension begins with prehypertension in persons aged 10-30 years (by increased cardiac output); then advances to early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent); then progresses to established hypertension in persons aged 30-50 years; and finally advances to complicated hypertension in persons aged 40-60 years. […] Patients who develop hypertension are known to develop a systemic hypertensive response secondary to vasoconstrictive stimuli. Alterations in structural and physical properties of resistance arteries, as well as changes in endothelial function, are probably responsible for this abnormal behavior of the vasculature. […] Furthermore, vascular remodeling occurs over the years as hypertension evolves, thereby maintaining increased vascular resistance irrespective of the initial hemodynamic pattern.

• #35 Signaling pathways in vascular function and hypertension: molecular mechanisms and therapeutic interventions | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-023-01430-7

  The NO-NOsGC-cGMP pathway is closely linked to the contractile function of VSMCs, and its activation precedes the development of hypertension. […] Vascular remodeling presents as vascular lumen narrowing, vascular wall thickening, and elasticity loss. […] Abnormal vascular structure is an important cause of hypertension and cardiovascular events. […] The changes of ECM mainly occur in the media, which may be related to the different SMC phenotypes and different secretory factors from SMCs. […] The renin-angiotensin-aldosterone system (RAAS) plays a critical role in the regulation of BP. […] The signaling pathways of RAAS in cells begin with the activation of various receptors, and the diverse effects of RAAS can be attributed to the activation of different receptors. […] The innate immunity serves as the initial defense against infectious agents and also contributes significantly to the development of sterile inflammation. […] The activation of muscle sympathetic nerve activity (SNA) is the key mechanism of sympathetic dysregulation leading to hypertension.

• #36 Advances in pathogenesis and treatment of essential hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9616110/

  Therefore, factors that cause increases in blood volume or decreases in vasodilation capacity can lead to hypertension. […] The most commonly applied method of controlling hypertension is pharmacological treatment based on lifestyle intervention. […] Currently, a lot of new findings about essential hypertension have emerged, and these provide important theoretical evidence to help develop a better understanding and treatment of essential hypertension. […] Arterial stiffness has been closely associated with an increased risk of essential hypertension, especially the isolated systolic hypertension. […] It is still a chicken and egg question that elevated blood pressure and arterial stiffness which come first. […] Structural arterial stiffness is closely associated with age, hyperlipidemia, diabetes mellitus, and is characterized by elastin disruption, collagen deposition, and altered extracellular matrix composition.

• #37 Advances in pathogenesis and treatment of essential hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9616110/

  Therefore, factors that cause increases in blood volume or decreases in vasodilation capacity can lead to hypertension. […] The most commonly applied method of controlling hypertension is pharmacological treatment based on lifestyle intervention. […] Currently, a lot of new findings about essential hypertension have emerged, and these provide important theoretical evidence to help develop a better understanding and treatment of essential hypertension. […] Arterial stiffness has been closely associated with an increased risk of essential hypertension, especially the isolated systolic hypertension. […] It is still a chicken and egg question that elevated blood pressure and arterial stiffness which come first. […] Structural arterial stiffness is closely associated with age, hyperlipidemia, diabetes mellitus, and is characterized by elastin disruption, collagen deposition, and altered extracellular matrix composition.

• #38 Advances in pathogenesis and treatment of essential hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9616110/

  Therefore, factors that cause increases in blood volume or decreases in vasodilation capacity can lead to hypertension. […] The most commonly applied method of controlling hypertension is pharmacological treatment based on lifestyle intervention. […] Currently, a lot of new findings about essential hypertension have emerged, and these provide important theoretical evidence to help develop a better understanding and treatment of essential hypertension. […] Arterial stiffness has been closely associated with an increased risk of essential hypertension, especially the isolated systolic hypertension. […] It is still a chicken and egg question that elevated blood pressure and arterial stiffness which come first. […] Structural arterial stiffness is closely associated with age, hyperlipidemia, diabetes mellitus, and is characterized by elastin disruption, collagen deposition, and altered extracellular matrix composition.

• #39 High Blood Pressure – Heart and Blood Vessel Disorders – Merck Manual Consumer Version

  https://www.merckmanuals.com/home/heart-and-blood-vessel-disorders/high-blood-pressure/high-blood-pressure

  High blood pressure (hypertension) is persistently high pressure in the arteries. […] Often no cause for high blood pressure can be identified, but sometimes it occurs as a result of an underlying disorder of the kidneys or a hormonal disorder. […] Obesity, a sedentary lifestyle, stress, smoking, and excessive amounts of alcohol or sodium (salt) in the diet all can play a role in the development of high blood pressure in people who have an inherited tendency to develop it. […] Changes due to aging may contribute to high blood pressure with no known cause (primary hypertension). As people age, large arteries gradually stiffen and small arteries may become partially blocked. Some experts think that this stiffening, combined with the narrowing of small arteries, may partly explain why blood pressure increases as people age.

• #40 Studying new-borns to understand the causes of high blood pressure – BHF

  https://www.bhf.org.uk/research-projects/the-role-of-capillary-rarefaction-in-the-pathogenesis-of-essential-hypertension-insights-from-studies-in-new-born-infants

  Adults with high blood pressure have a high risk of developing cardiovascular disease, or of having a heart attack or stroke. […] Understanding the causes of high blood pressure is vital to developing new treatments to prevent these life-threatening conditions. […] If these [capillaries and arterioles] become damaged, high blood pressure can develop. […] An important abnormality that may develop is a reduced number of these tiny vessels in a particular part of the circulation. […] The research team will study new-born babies who are at risk of developing high blood pressure later in life, because they have a low birth weight or their mother has high blood pressure. […] This research will benefit not only affected new-borns, but will also apply to understanding and improving the treatment of high blood pressure in adults.

• #41 Primary Role of the Kidney in Pathogenesis of Hypertension

  https://www.mdpi.com/2075-1729/14/1/119

  Previous transplantation studies and the concept of ‘nephron underdosing’ support the idea that the kidney plays a crucial role in the development of essential hypertension. […] Hypertension is induced when the pressure-natriuresis mechanism fails due to both subtle and overt kidney abnormalities. […] The renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS) are the major regulators of renal sodium reabsorption. […] Sodium overload, caused by increased intake and/or reduced renal excretion, not only leads to an expansion of plasma volume but also to an increase in systemic vascular resistance. […] Endothelial dysfunction is caused by an increased intracellular Na+ concentration, which inhibits endothelial nitric oxide (NO) synthase and reduces NO production. […] In conclusion, the primary cause of hypertension is sodium overload resulting from kidney dysregulation.

• #42 Pathophysiology of Hypertension: Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension

  https://emedicine.medscape.com/article/1937383-overview

  The progression of essential hypertension begins with prehypertension in persons aged 10-30 years (by increased cardiac output); then advances to early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent); then progresses to established hypertension in persons aged 30-50 years; and finally advances to complicated hypertension in persons aged 40-60 years. […] Patients who develop hypertension are known to develop a systemic hypertensive response secondary to vasoconstrictive stimuli. Alterations in structural and physical properties of resistance arteries, as well as changes in endothelial function, are probably responsible for this abnormal behavior of the vasculature. […] Furthermore, vascular remodeling occurs over the years as hypertension evolves, thereby maintaining increased vascular resistance irrespective of the initial hemodynamic pattern.

• #43 High blood pressure (hypertension) – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/symptoms-causes/syc-20373410

  This type of high blood pressure is caused by an underlying condition. It tends to appear suddenly and cause higher blood pressure than does primary hypertension. Conditions and medicines that can lead to secondary hypertension include: Adrenal gland tumors, Blood vessel problems present at birth, also called congenital heart defects, Cough and cold medicines, some pain relievers, birth control pills, and other prescription drugs, Illegal drugs, such as cocaine and amphetamines, Kidney disease, Obstructive sleep apnea, Thyroid problems. […] The excessive pressure on the artery walls caused by high blood pressure can damage blood vessels and body organs. The higher the blood pressure and the longer it goes uncontrolled, the greater the damage. […] Uncontrolled high blood pressure can lead to complications including: Heart attack or stroke, Aneurysm, Heart failure, Kidney problems, Eye problems, Metabolic syndrome, Changes with memory or understanding, Dementia.

• #44 Blood pressure and heart failure | Clinical Hypertension | Full Text

  https://clinicalhypertension.biomedcentral.com/articles/10.1186/s40885-019-0132-x

  Hypertension is a leading cause of cardiovascular disease, stroke, and death. It affects a substantial proportion of the population worldwide, and remains underdiagnosed and undertreated. […] Long-standing high blood pressure leads to left ventricular hypertrophy and diastolic dysfunction that cause an increase in myocardial rigidity, which renders the myocardium less compliant to changes in the preload, afterload, and sympathetic tone. […] Chronic HTN causes structural and functional changes in the heart that ultimately lead to HF, which further increases mortality and morbidity. […] High BP increases the left ventricular (LV) afterload and peripheral vascular resistance, and prolonged exposure to an increased load leads to pressure- and volume-mediated LV structural remodeling. […] Diastolic dysfunction is one of the first changes observed in a heart that has been exposed to an increased load.

• #45 Hypertension – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/hypertension/hypertension

  The renin-angiotensin-aldosterone system helps regulate blood volume and therefore blood pressure. […] Elevated angiotensin II levels are generally acknowledged to be responsible for renovascular hypertension, at least in the early phase, but the role of the renin-angiotensin-aldosterone system in primary hypertension is not established. […] Deficiency of a vasodilator (eg, bradykinin, nitric oxide), rather than excess of a vasoconstrictor (eg, angiotensin, norepinephrine), may cause hypertension. […] No pathologic changes occur early in hypertension. Severe or prolonged hypertension damages target organs (primarily the cardiovascular system, brain, and kidneys), increasing risk of […] Coronary artery disease (CAD) and myocardial infarction (MI) […] Heart failure […] Stroke (particularly hemorrhagic)

• #46 Blood pressure and heart failure | Clinical Hypertension | Full Text

  https://clinicalhypertension.biomedcentral.com/articles/10.1186/s40885-019-0132-x

  The pathway from LV hypertrophy to overt HF is complex and unclear. […] The presence of an LV strain pattern, that is, LV hypertrophy, on a 12-lead electrocardiogram is an independent predictor of the CV outcome. […] Patients with long-standing HTN are more sensitive to changes in pressure, volume, and sympathetic tone. […] The relationship between BP and the HF prognosis is not necessarily always linear. […] The findings from a study of the KorAHF registry showed that a reverse J-curve relationship was evident between the treatment of BP and the outcomes of patients who were hospitalized for HF. […] The current evidence suggests that all patients with HF should receive triple therapy comprising ACE inhibitors or ARBs, beta-blockers, and diuretics, with the doses adjusted to maintain an adequate BP, and if a patient remains hypertensive, thiazide-like diuretics can be added.

• #47 Etiology and management of hypertension in patients with cancer | Cardio-Oncology | Full Text

  https://cardiooncologyjournal.biomedcentral.com/articles/10.1186/s40959-021-00101-2

  Another hypothesis is that angiotensin II, which is elevated in hypertensive patients, can stimulate the production of vascular endothelial growth factor (VEGF), which in turn augments cancer-related angiogenesis. […] Hypertension leads to increased systemic vascular resistance, which in turn leads to pressure overload. Increased left ventricular wall stress results in the release of growth factors and cytokines, which then leads to concentric remodeling and hypertrophy. […] Hypertension-mediated cytokine activation can also increase the rate of downstream cell apoptosis, leading to ventricular dysfunction. […] Therefore, preexisting hypertension may worsen the overall prognosis of patients undergoing anthracycline-based chemotherapy and/or trastuzumab. Effective treatment of hypertension allows the patients to tolerate maximum doses of the planned cancer therapy, yielding better control of the tumor.

• #48 High Blood Pressure and Your Kidneys | American Heart Association

  https://www.heart.org/en/health-topics/high-blood-pressure/health-threats-from-high-blood-pressure/high-blood-pressure-and-your-kidneys

  Uncontrolled high blood pressure can damage your kidneys. […] Over time, uncontrolled high blood pressure can cause arteries in and around the kidneys to narrow, weaken or harden. […] When those blood vessels become damaged, the kidneys don’t receive the oxygen and nutrients they need to work well. High blood pressure can lead to scarring of kidney tissue. This can impair how kidneys are able to filter the blood and how they regulate fluid and electrolytes. This results in high blood pressure that is more difficult to control. […] Damaged kidney arteries don’t filter blood well. Delicate blood vessels within the kidney filter the blood. When the kidney becomes damaged from high blood pressure, these blood vessels don’t receive needed oxygen and nutrients. Then the kidneys cannot filter blood. They also can’t regulate fluid, hormones, acids and salts in the body.

• #49 About High Blood Pressure | High Blood Pressure | CDC

  https://www.cdc.gov/high-blood-pressure/about/index.html

  High blood pressure can cause the arteries that supply blood and oxygen to the brain to burst or be blocked, causing a stroke. […] High blood pressure can cause heart valve disease, which is when any valve in the heart is damaged or diseased. […] Adults with diabetes, high blood pressure, or both have a higher risk of developing chronic kidney disease than those without these conditions. […] By taking action to lower your blood pressure, you can help protect yourself against heart disease and stroke, also called cardiovascular disease (CVD).

• #50 High Blood Pressure and Your Kidneys | American Heart Association

  https://www.heart.org/en/health-topics/high-blood-pressure/health-threats-from-high-blood-pressure/high-blood-pressure-and-your-kidneys

  Damaged kidneys fail to regulate blood pressure. Healthy kidneys respond to a hormone called aldosterone. This hormone plays an important role in regulating blood pressure throughout the body. But kidney damage and uncontrolled high blood pressure can create a harmful cycle. Blood pressure can become more difficult to control in people with kidney damage, and uncontrolled high blood pressure can contribute to worsening kidney damage. […] Kidney failure due to high blood pressure can take years to develop. You can limit your risk by managing your blood pressure.

• #51 High blood pressure | Stroke Association

  https://www.stroke.org.uk/stroke/managing-risk/high-blood-pressure

  High blood pressure is the biggest single risk factor for stroke. It plays a part in about half of all strokes. But while high blood pressure is a serious condition, there are things you can do to reduce your risk of a stroke. […] High blood pressure can lead to stroke in different ways. It can lead to blood clots in the brain and can damage the tiny blood vessels deep inside the brain. It can also make a stroke, due to bleeding in the brain, more likely. […] High blood pressure damages your blood vessels by making them become narrower and stiffer, and causing a build-up of fatty material. This process is called atherosclerosis. Clots can form on the areas of fatty material, and if a clot travels to the brain, it causes an ischaemic stroke or transient ischaemic attack (TIA or mini-stroke). […] High blood pressure can damage blood vessels inside the brain, causing bleeding in the brain. This is called a haemorrhagic stroke. […] High blood pressure over a long time is a risk factor for small vessel disease.

• #52 High blood pressure (hypertension) – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/symptoms-causes/syc-20373410

  This type of high blood pressure is caused by an underlying condition. It tends to appear suddenly and cause higher blood pressure than does primary hypertension. Conditions and medicines that can lead to secondary hypertension include: Adrenal gland tumors, Blood vessel problems present at birth, also called congenital heart defects, Cough and cold medicines, some pain relievers, birth control pills, and other prescription drugs, Illegal drugs, such as cocaine and amphetamines, Kidney disease, Obstructive sleep apnea, Thyroid problems. […] The excessive pressure on the artery walls caused by high blood pressure can damage blood vessels and body organs. The higher the blood pressure and the longer it goes uncontrolled, the greater the damage. […] Uncontrolled high blood pressure can lead to complications including: Heart attack or stroke, Aneurysm, Heart failure, Kidney problems, Eye problems, Metabolic syndrome, Changes with memory or understanding, Dementia.

• #53 High blood pressure | Stroke Association

  https://www.stroke.org.uk/stroke/managing-risk/high-blood-pressure

  High blood pressure is the biggest single risk factor for stroke. It plays a part in about half of all strokes. But while high blood pressure is a serious condition, there are things you can do to reduce your risk of a stroke. […] High blood pressure can lead to stroke in different ways. It can lead to blood clots in the brain and can damage the tiny blood vessels deep inside the brain. It can also make a stroke, due to bleeding in the brain, more likely. […] High blood pressure damages your blood vessels by making them become narrower and stiffer, and causing a build-up of fatty material. This process is called atherosclerosis. Clots can form on the areas of fatty material, and if a clot travels to the brain, it causes an ischaemic stroke or transient ischaemic attack (TIA or mini-stroke). […] High blood pressure can damage blood vessels inside the brain, causing bleeding in the brain. This is called a haemorrhagic stroke. […] High blood pressure over a long time is a risk factor for small vessel disease.

• #54 The pathophysiology of hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC1120075/

  Epidemiologically there is a clustering of several risk factors, including obesity, hypertension, glucose intolerance, diabetes mellitus, and hyperlipidaemia. […] Although separate genes and genetic factors have been linked to the development of essential hypertension, multiple genes are most likely contribute to the development of the disorder in a particular individual. […] Some specific genetic mutations can rarely cause hypertension. Experimental models of genetic hypertension have shown that the inherited tendency to hypertension resides primarily in the kidney. […] There is increasing evidence that fetal influences, particularly birth weight, may be a determinant of blood pressure in adult life.

• #55 Decoding the mechanism of hypertension through multiomics profiling | Journal of Human Hypertension

  https://www.nature.com/articles/s41371-022-00769-8

  Genes have been identified to underlie key mechanisms in the pathophysiology of hypertension including those involved in the RAAS, catecholamine/adrenergic system, renal kallikreinkinin system, epithelial sodium channel, adducin, and those involving lipoprotein metabolism, hormone receptors, and growth factors. […] Genome-wide association studies (GWAS) have transformed the study of complex disease genetics by testing millions of genetic variants throughout the genomes of individuals to find genotype-phenotype relationships. […] GWAS have identified genetic variants in hypertension and have enabled an understanding of the traits that underlie hypertension. […] The major bottle neck is associating SNP to causal genes and function. […] The advent of technologies has allowed the genetic analysis possible, and disease-causing variants can be detected.

• #56 Hypertension: MedlinePlus GeneticsLock

  https://medlineplus.gov/genetics/condition/hypertension/

  Hypertension can have a variety of causes. Secondary hypertension results from other disorders that raise blood pressure in addition to other problems. Rare, genetic forms of hypertension are caused by mutations in particular genes, many of which help control the balance of fluids and salts in the body and affect blood pressure. The causes of essential hypertension, however, are not well understood. Essential hypertension is a complex condition with a variety of factors, both genetic and environmental, contributing to its development. […] More than 100 genetic variations have been associated with essential hypertension. While these variations have been found more commonly in people with essential hypertension than in unaffected individuals, none are common causes of the condition. […] The most-studied genetic association in essential hypertension is with genes involved in the renin-angiotensin-aldosterone system. The renin-angiotensin-aldosterone system is a step-wise process that produces hormones to regulate blood pressure and the balance of fluids and salts in the body.

• #57 Hypertension: MedlinePlus GeneticsLock

  https://medlineplus.gov/genetics/condition/hypertension/

  Hypertension can have a variety of causes. Secondary hypertension results from other disorders that raise blood pressure in addition to other problems. Rare, genetic forms of hypertension are caused by mutations in particular genes, many of which help control the balance of fluids and salts in the body and affect blood pressure. The causes of essential hypertension, however, are not well understood. Essential hypertension is a complex condition with a variety of factors, both genetic and environmental, contributing to its development. […] More than 100 genetic variations have been associated with essential hypertension. While these variations have been found more commonly in people with essential hypertension than in unaffected individuals, none are common causes of the condition. […] The most-studied genetic association in essential hypertension is with genes involved in the renin-angiotensin-aldosterone system. The renin-angiotensin-aldosterone system is a step-wise process that produces hormones to regulate blood pressure and the balance of fluids and salts in the body.

• #58 Genetic Factors Contributing to the Pathogenesis of Essential Hypertension in Two African Populations

  https://www.mdpi.com/2075-4426/14/3/323

  The African continent has the highest prevalence of hypertension globally, with South Africa reporting the highest prevalence in Southern Africa. […] This study aimed to assess the association of genetic variants and essential hypertension in a cohort of two ethnic South African population groups. […] Five variants (CYP11B2 rs179998, AGT rs5051 and rs699, AGTR1 rs5186, and ACE rs4646994) were significantly associated with essential hypertension in the cohort under study. […] Furthermore, AGTR1 rs5186 and AGT rs699 were identified as risk factors for the development of hypertension in both ethnic groups. […] In two ethnic South African populations, an association was observed between renin–angiotensin–aldosterone system (RAAS)-related genes and the development of hypertension. […] Despite the clinical differences observed in hypertensive patients of African descent, a limited number of studies have investigated genetic factors contributing to the pathogenesis of EH in these populations.

• #59 Genetic Factors Contributing to the Pathogenesis of Essential Hypertension in Two African Populations

  https://www.mdpi.com/2075-4426/14/3/323

  The Sodium Retention Hypothesis suggests that, evolutionarily, the capacity to retain salt provided a biological advantage and increased the fitness of salt retainers in tropical hunter-gatherer societies. […] Our investigation identified significant associations between EH and five variants in genes related to the renin–angiotensin–aldosterone system (RAAS): CYP11B2 rs179998, AGT rs5051, AGT rs699, AGTR1 rs5186, and ACE rs4646994. […] The observed associations between RAAS variants and EH in our study support the Sodium Retention Hypothesis and highlight the need for pharmacogenetic research of anti-hypertensive treatment in these population groups. […] The ACE gene’s rs4646994 variant, an insertion/deletion polymorphism, unveiled opposing associations with EH, echoing the complex nature of genetic influences on BP regulation.

• #60 Hypertension: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/241381-overview

  Investigations into the pathophysiology of hypertension, both in animals and humans, have revealed that hypertension may have an immunologic basis. […] Studies have revealed that hypertension is associated with renal infiltration of immune cells and that pharmacologic immunosuppression (such as with the drug mycophenolate mofetil) or pathologic immunosuppression (such as occurs with human immunovirus [HIV] deficiency) results in reduced BP in animals and humans. […] Evidence suggests that T lymphocytes and T-cell derived cytokines (eg, interleukin 17, tumor necrosis factor alpha) play an important role in hypertension. […] One hypothesis is that prehypertension results in oxidation of lipids such as arachidonic acid that leads to the formation of isoketals or isolevuglandins, which function as neoantigens, which are then presented to T cells, leading to T-cell activation and infiltration of critical organs (eg, kidney, vasculature). […] This results in persistent or severe hypertension and end-organ damage.

• #61 Hypertension: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/241381-overview

  Investigations into the pathophysiology of hypertension, both in animals and humans, have revealed that hypertension may have an immunologic basis. […] Studies have revealed that hypertension is associated with renal infiltration of immune cells and that pharmacologic immunosuppression (such as with the drug mycophenolate mofetil) or pathologic immunosuppression (such as occurs with human immunovirus [HIV] deficiency) results in reduced BP in animals and humans. […] Evidence suggests that T lymphocytes and T-cell derived cytokines (eg, interleukin 17, tumor necrosis factor alpha) play an important role in hypertension. […] One hypothesis is that prehypertension results in oxidation of lipids such as arachidonic acid that leads to the formation of isoketals or isolevuglandins, which function as neoantigens, which are then presented to T cells, leading to T-cell activation and infiltration of critical organs (eg, kidney, vasculature). […] This results in persistent or severe hypertension and end-organ damage.

• #62 Hypertension: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/241381-overview

  Investigations into the pathophysiology of hypertension, both in animals and humans, have revealed that hypertension may have an immunologic basis. […] Studies have revealed that hypertension is associated with renal infiltration of immune cells and that pharmacologic immunosuppression (such as with the drug mycophenolate mofetil) or pathologic immunosuppression (such as occurs with human immunovirus [HIV] deficiency) results in reduced BP in animals and humans. […] Evidence suggests that T lymphocytes and T-cell derived cytokines (eg, interleukin 17, tumor necrosis factor alpha) play an important role in hypertension. […] One hypothesis is that prehypertension results in oxidation of lipids such as arachidonic acid that leads to the formation of isoketals or isolevuglandins, which function as neoantigens, which are then presented to T cells, leading to T-cell activation and infiltration of critical organs (eg, kidney, vasculature). […] This results in persistent or severe hypertension and end-organ damage.

• #63 Hypertension: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/241381-overview

  Investigations into the pathophysiology of hypertension, both in animals and humans, have revealed that hypertension may have an immunologic basis. […] Studies have revealed that hypertension is associated with renal infiltration of immune cells and that pharmacologic immunosuppression (such as with the drug mycophenolate mofetil) or pathologic immunosuppression (such as occurs with human immunovirus [HIV] deficiency) results in reduced BP in animals and humans. […] Evidence suggests that T lymphocytes and T-cell derived cytokines (eg, interleukin 17, tumor necrosis factor alpha) play an important role in hypertension. […] One hypothesis is that prehypertension results in oxidation of lipids such as arachidonic acid that leads to the formation of isoketals or isolevuglandins, which function as neoantigens, which are then presented to T cells, leading to T-cell activation and infiltration of critical organs (eg, kidney, vasculature). […] This results in persistent or severe hypertension and end-organ damage.

• #64 Hypertension: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/241381-overview

  Investigations into the pathophysiology of hypertension, both in animals and humans, have revealed that hypertension may have an immunologic basis. […] Studies have revealed that hypertension is associated with renal infiltration of immune cells and that pharmacologic immunosuppression (such as with the drug mycophenolate mofetil) or pathologic immunosuppression (such as occurs with human immunovirus [HIV] deficiency) results in reduced BP in animals and humans. […] Evidence suggests that T lymphocytes and T-cell derived cytokines (eg, interleukin 17, tumor necrosis factor alpha) play an important role in hypertension. […] One hypothesis is that prehypertension results in oxidation of lipids such as arachidonic acid that leads to the formation of isoketals or isolevuglandins, which function as neoantigens, which are then presented to T cells, leading to T-cell activation and infiltration of critical organs (eg, kidney, vasculature). […] This results in persistent or severe hypertension and end-organ damage.

• #65 The participation of immunity in the pathogenesis of arterial hypertension | Nefrología

  https://www.revistanefrologia.com/en-the-participation-immunity-in-pathogenesis-articulo-S2013251420300110

  Studies conducted to demonstrate the participation of the immune system in the pathogenesis of hypertension are relatively recent. […] It has been during the most recent decades that a growing number of studies were conducted to unequivocally establish the critical role of autoimmunity in the complex aetiopathogenetic mechanism resulting in high blood pressure. […] It is well established that inflammation at the levels of the kidney, artery wall, and the central nervous system promotes and increases the severity of hypertension. […] The role of lymphocytes in the pathogenesis of hypertension was initially observed in pioneering experiments by Svendsen, who demonstrated that nude (athymic) mice did not develop salt-dependent hypertension in the DOCA (deoxycorticosterone)-salt model. […] Innate immunity, acquired immunity, and autoimmunity play an important role in hypertension.

• #66 Can An Infection Cause High Blood Pressure?

  https://revivalresearch.org/blogs/can-an-infection-cause-high-blood-pressure/

  High blood pressure, or hypertension, is a medical condition where the force of the blood against the walls of the arteries is consistently too high. […] The connection between infections and high blood pressure is one area that has gained attention from multiple clinical research organizations. […] To understand the potential link between infections and high blood pressure, its important to delve into the basics of hypertension, its causes, and the intricate mechanisms that govern our cardiovascular system. […] Chronic infections can cause persistent inflammation and can lead to endothelial dysfunction. This malfunction impairs the ability of blood vessels to relax and contract properly, contributing to high blood pressure. […] Some infections can activate the RAAS, a hormonal system that regulates blood pressure and fluid balance. Excessive activation of this system can result in vasoconstriction (narrowing of blood vessels) and sodium retention, both of which contribute to high blood pressure.

• #67 Pathophysiology of Hypertension: Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension

  https://emedicine.medscape.com/article/1937383-overview

  The progression of essential hypertension begins with prehypertension in persons aged 10-30 years (by increased cardiac output); then advances to early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent); then progresses to established hypertension in persons aged 30-50 years; and finally advances to complicated hypertension in persons aged 40-60 years. […] Patients who develop hypertension are known to develop a systemic hypertensive response secondary to vasoconstrictive stimuli. Alterations in structural and physical properties of resistance arteries, as well as changes in endothelial function, are probably responsible for this abnormal behavior of the vasculature. […] Furthermore, vascular remodeling occurs over the years as hypertension evolves, thereby maintaining increased vascular resistance irrespective of the initial hemodynamic pattern.

• #68 Hypertension: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/241381-overview

  A general progression of primary hypertension is as follows: Prehypertension in persons aged 10-30 years (by increased cardiac output), Early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent), Established hypertension in persons aged 30-50 years, Complicated hypertension in persons aged 40-60 years. […] As evident from the above, younger individuals may present with hypertension associated with an elevated cardiac output (high-output hypertension). High-output hypertension results from volume and sodium retention by the kidney, leading to increased stroke volume and, often, with cardiac stimulation by adrenergic hyperactivity. […] Systemic vascular resistance is generally not increased at such earlier stages of hypertension. As hypertension is sustained, however, vascular adaptations including remodeling, vasoconstriction, and vascular rarefaction occur, leading to increased systemic vascular resistance.

• #69 Hypertension: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/241381-overview

  A general progression of primary hypertension is as follows: Prehypertension in persons aged 10-30 years (by increased cardiac output), Early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent), Established hypertension in persons aged 30-50 years, Complicated hypertension in persons aged 40-60 years. […] As evident from the above, younger individuals may present with hypertension associated with an elevated cardiac output (high-output hypertension). High-output hypertension results from volume and sodium retention by the kidney, leading to increased stroke volume and, often, with cardiac stimulation by adrenergic hyperactivity. […] Systemic vascular resistance is generally not increased at such earlier stages of hypertension. As hypertension is sustained, however, vascular adaptations including remodeling, vasoconstriction, and vascular rarefaction occur, leading to increased systemic vascular resistance.

• #70 Hypertension: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/241381-overview

  A general progression of primary hypertension is as follows: Prehypertension in persons aged 10-30 years (by increased cardiac output), Early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent), Established hypertension in persons aged 30-50 years, Complicated hypertension in persons aged 40-60 years. […] As evident from the above, younger individuals may present with hypertension associated with an elevated cardiac output (high-output hypertension). High-output hypertension results from volume and sodium retention by the kidney, leading to increased stroke volume and, often, with cardiac stimulation by adrenergic hyperactivity. […] Systemic vascular resistance is generally not increased at such earlier stages of hypertension. As hypertension is sustained, however, vascular adaptations including remodeling, vasoconstriction, and vascular rarefaction occur, leading to increased systemic vascular resistance.

• #71 Pathophysiology of Hypertension: Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension

  https://emedicine.medscape.com/article/1937383-overview

  An elevated level of uric acid may also be an independent factor of diastolic dysfunction in apparently healthy individuals with essential hypertension but without heart failure. […] Over the course of its natural history, essential hypertension progresses from occasional to established hypertension. After a long, invariable, asymptomatic period, persistent hypertension develops into complicated hypertension, in which target organ damage to the aorta and small arteries, heart, kidneys, retina, and central nervous system is evident. […] There is also an association between hypertension and malignancy, in which overlapping risk factors (eg, higher body mass index, tobacco and/or alcohol use, physical inactivity, unhealthy diet) and pathophysiologic mechanisms (eg, immunoinflammation, oxidative stress) exist.

• #72 Hypertension: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/241381-overview

  The pathogenesis of primary hypertension is multifactorial and complex. […] Multiple factors modulate the blood pressure (BP) including humoral mediators, vascular reactivity, circulating blood volume, vascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and neural stimulation. The pathogenesis of primary hypertension involves multiple factors, including genetic predisposition, excess dietary salt intake, adrenergic tone, and renal sodium and water handling that interact to produce BP elevations. […] Emerging evidence suggests a role for immune cell activation and the microbiome in the pathogenesis of hypertension. […] The natural history of primary hypertension evolves from occasional to established hypertension. After a long asymptomatic period, persistent hypertension develops into complicated hypertension, in which end-organ damage to the aorta and small arteries, heart, kidneys, retina, and central nervous system is evident.

• #73 Diagnosing Secondary Hypertension | AAFP

  https://www.aafp.org/pubs/afp/issues/2003/0101/p67.html

  Secondary hypertension is elevated blood pressure that results from an underlying, identifiable, often correctable cause. […] Patients with hypertension have some underlying mechanism that elevates their blood pressure. […] Although only about 5 to 10 percent of hypertension cases are thought to result from secondary causes, hypertension is so common that secondary hypertension probably will be encountered frequently by the primary care practitioner. […] The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-VI) defines four goals for the evaluation of the patient with elevated blood pressure: detection and confirmation of hypertension; detection of target organ disease (e.g., renal damage, congestive heart failure); identification of other risk factors for cardiovascular disorders (e.g., diabetes mellitus, hyperlipidemia); and detection of secondary causes of hypertension.

• #74 Diagnosing Secondary Hypertension | AAFP

  https://www.aafp.org/pubs/afp/issues/2003/0101/p67.html

  Secondary hypertension is elevated blood pressure that results from an underlying, identifiable, often correctable cause. […] Patients with hypertension have some underlying mechanism that elevates their blood pressure. […] Although only about 5 to 10 percent of hypertension cases are thought to result from secondary causes, hypertension is so common that secondary hypertension probably will be encountered frequently by the primary care practitioner. […] The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-VI) defines four goals for the evaluation of the patient with elevated blood pressure: detection and confirmation of hypertension; detection of target organ disease (e.g., renal damage, congestive heart failure); identification of other risk factors for cardiovascular disorders (e.g., diabetes mellitus, hyperlipidemia); and detection of secondary causes of hypertension.

• #75 CV Physiology | Secondary Hypertension

  https://cvphysiology.com/blood-pressure/bp023

  Secondary hypertension accounts for approximately 5-10% of all cases of hypertension, with the remaining being primary hypertension. Secondary hypertension has an identifiable cause, whereas primary hypertension has no known cause (idiopathic). […] Regardless of the cause, arterial pressure becomes elevated because of an increase in cardiac output, an increase in systemic vascular resistance, or both. […] Increased systemic vascular resistance is most commonly caused, at least initially, by increased sympathetic activation or by the effects of circulating vasoconstrictors (e.g., angiotensin II). […] Renovascular hypertensionRenal artery disease can cause narrowing of the vessel lumen (stenosis). The reduced lumen diameter decreases the pressure at the afferent arteriole in the kidney and reduces renal perfusion. This stimulates renin release by the kidney, which increases circulating angiotensin II (AII) and aldosterone. These hormones increase blood volume by enhancing renal reabsorption of sodium and water, which increases cardiac output (CO) by the Frank-Starling mechanism. Increased AII also causes systemic vasoconstriction (SVR) and enhances sympathetic activity, and chronic elevation of AII promotes cardiac and vascular hypertrophy. Therefore, hypertension caused by renal artery stenosis results from both an increase in systemic vascular resistance and an increase in cardiac output.

• #76 CV Physiology | Secondary Hypertension

  https://cvphysiology.com/blood-pressure/bp023

  Secondary hypertension accounts for approximately 5-10% of all cases of hypertension, with the remaining being primary hypertension. Secondary hypertension has an identifiable cause, whereas primary hypertension has no known cause (idiopathic). […] Regardless of the cause, arterial pressure becomes elevated because of an increase in cardiac output, an increase in systemic vascular resistance, or both. […] Increased systemic vascular resistance is most commonly caused, at least initially, by increased sympathetic activation or by the effects of circulating vasoconstrictors (e.g., angiotensin II). […] Renovascular hypertensionRenal artery disease can cause narrowing of the vessel lumen (stenosis). The reduced lumen diameter decreases the pressure at the afferent arteriole in the kidney and reduces renal perfusion. This stimulates renin release by the kidney, which increases circulating angiotensin II (AII) and aldosterone. These hormones increase blood volume by enhancing renal reabsorption of sodium and water, which increases cardiac output (CO) by the Frank-Starling mechanism. Increased AII also causes systemic vasoconstriction (SVR) and enhances sympathetic activity, and chronic elevation of AII promotes cardiac and vascular hypertrophy. Therefore, hypertension caused by renal artery stenosis results from both an increase in systemic vascular resistance and an increase in cardiac output.

• #77 Diagnosing Secondary Hypertension | AAFP

  https://www.aafp.org/pubs/afp/issues/2003/0101/p67.html

  Obstructive sleep apnea (OSA), a repetitive mechanical obstruction of the upper airway during sleep, is an independent risk factor for hypertension. […] Primary hyperaldosteronism is defined as overproduction of aldosterone independent of its usual regulator, the renin-angiotensin system. […] Renovascular hypertension is defined as hypertension resulting from compromised arterial supply to the kidneys. […] Renal parenchymal disease can be a cause or consequence of hypertension. […] Excess catecholamine levels play a role in causing white-coat hypertension and hypertension in pheochromocytoma, OSA, and other diseases discussed in this article. […] Coarctation of the aorta is a congenital narrowing of the aortic lumen, most often occurring just distal to the origin of the left subclavian artery.

• #78 CV Physiology | Secondary Hypertension

  https://cvphysiology.com/blood-pressure/bp023

  Secondary hypertension accounts for approximately 5-10% of all cases of hypertension, with the remaining being primary hypertension. Secondary hypertension has an identifiable cause, whereas primary hypertension has no known cause (idiopathic). […] Regardless of the cause, arterial pressure becomes elevated because of an increase in cardiac output, an increase in systemic vascular resistance, or both. […] Increased systemic vascular resistance is most commonly caused, at least initially, by increased sympathetic activation or by the effects of circulating vasoconstrictors (e.g., angiotensin II). […] Renovascular hypertensionRenal artery disease can cause narrowing of the vessel lumen (stenosis). The reduced lumen diameter decreases the pressure at the afferent arteriole in the kidney and reduces renal perfusion. This stimulates renin release by the kidney, which increases circulating angiotensin II (AII) and aldosterone. These hormones increase blood volume by enhancing renal reabsorption of sodium and water, which increases cardiac output (CO) by the Frank-Starling mechanism. Increased AII also causes systemic vasoconstriction (SVR) and enhances sympathetic activity, and chronic elevation of AII promotes cardiac and vascular hypertrophy. Therefore, hypertension caused by renal artery stenosis results from both an increase in systemic vascular resistance and an increase in cardiac output.

• #79 CV Physiology | Secondary Hypertension

  https://cvphysiology.com/blood-pressure/bp023

  Secondary hypertension accounts for approximately 5-10% of all cases of hypertension, with the remaining being primary hypertension. Secondary hypertension has an identifiable cause, whereas primary hypertension has no known cause (idiopathic). […] Regardless of the cause, arterial pressure becomes elevated because of an increase in cardiac output, an increase in systemic vascular resistance, or both. […] Increased systemic vascular resistance is most commonly caused, at least initially, by increased sympathetic activation or by the effects of circulating vasoconstrictors (e.g., angiotensin II). […] Renovascular hypertensionRenal artery disease can cause narrowing of the vessel lumen (stenosis). The reduced lumen diameter decreases the pressure at the afferent arteriole in the kidney and reduces renal perfusion. This stimulates renin release by the kidney, which increases circulating angiotensin II (AII) and aldosterone. These hormones increase blood volume by enhancing renal reabsorption of sodium and water, which increases cardiac output (CO) by the Frank-Starling mechanism. Increased AII also causes systemic vasoconstriction (SVR) and enhances sympathetic activity, and chronic elevation of AII promotes cardiac and vascular hypertrophy. Therefore, hypertension caused by renal artery stenosis results from both an increase in systemic vascular resistance and an increase in cardiac output.

• #80 CV Physiology | Secondary Hypertension

  https://cvphysiology.com/blood-pressure/bp023

  Pathologic processes (e.g., diabetic nephropathy, glomerulonephritis) can damage nephrons in the kidney. When this occurs, the kidney cannot excrete normal amounts of sodium, which leads to sodium and water retention, increased blood volume, and increased cardiac output by the Frank-Starling mechanism. […] Increased circulating aldosterone causes renal retention of sodium and water, which causes blood volume and arterial pressure to increase. […] Emotional stress leads to activation of the sympathetic nervous system, which causes increased release of norepinephrine from sympathetic nerves in the heart and blood vessels, leading to increased cardiac output and increased systemic vascular resistance. […] The mechanism of hypertension may be related to sympathetic activation and hormonal changes associated with repeated periods of apnea-induced hypoxia and hypercapnia, and from stress associated with the loss of sleep.

• #81 CV Physiology | Secondary Hypertension

  https://cvphysiology.com/blood-pressure/bp023

  Pathologic processes (e.g., diabetic nephropathy, glomerulonephritis) can damage nephrons in the kidney. When this occurs, the kidney cannot excrete normal amounts of sodium, which leads to sodium and water retention, increased blood volume, and increased cardiac output by the Frank-Starling mechanism. […] Increased circulating aldosterone causes renal retention of sodium and water, which causes blood volume and arterial pressure to increase. […] Emotional stress leads to activation of the sympathetic nervous system, which causes increased release of norepinephrine from sympathetic nerves in the heart and blood vessels, leading to increased cardiac output and increased systemic vascular resistance. […] The mechanism of hypertension may be related to sympathetic activation and hormonal changes associated with repeated periods of apnea-induced hypoxia and hypercapnia, and from stress associated with the loss of sleep.

• #82 Diagnosing Secondary Hypertension | AAFP

  https://www.aafp.org/pubs/afp/issues/2003/0101/p67.html

  Obstructive sleep apnea (OSA), a repetitive mechanical obstruction of the upper airway during sleep, is an independent risk factor for hypertension. […] Primary hyperaldosteronism is defined as overproduction of aldosterone independent of its usual regulator, the renin-angiotensin system. […] Renovascular hypertension is defined as hypertension resulting from compromised arterial supply to the kidneys. […] Renal parenchymal disease can be a cause or consequence of hypertension. […] Excess catecholamine levels play a role in causing white-coat hypertension and hypertension in pheochromocytoma, OSA, and other diseases discussed in this article. […] Coarctation of the aorta is a congenital narrowing of the aortic lumen, most often occurring just distal to the origin of the left subclavian artery.

• #83 CV Physiology | Secondary Hypertension

  https://cvphysiology.com/blood-pressure/bp023

  Elevated thyroxin levels cause increased blood volume through activation of the renin-angiotensin-aldosterone system, and increased heart rate and ventricular contractility. […] Catecholamine secreting tumors in the adrenal medulla can lead to very high levels of circulating catecholamines (both epinephrine and norepinephrine). This leads to alpha-adrenoceptor mediated systemic vasoconstriction and beta-adrenoceptor mediated cardiac stimulation, both of which contribute to significant elevations in arterial pressure. […] This is a serious condition that sometimes develops during the third trimester of pregnancy that causes hypertension due to increased blood volume, which increases cardiac output by the Frank-Starling mechanism. […] Obstruction of the aorta at this point reduces distal arterial pressures and elevates arterial pressures in the head and arms. The reduced systemic arterial pressure activates the renin-angiotensin-aldosterone system, which leads to an increase in blood volume, which further increases arterial pressures in the upper body and may largely offset the reduction in lower body arterial pressures.

• #84 CV Physiology | Secondary Hypertension

  https://cvphysiology.com/blood-pressure/bp023

  Elevated thyroxin levels cause increased blood volume through activation of the renin-angiotensin-aldosterone system, and increased heart rate and ventricular contractility. […] Catecholamine secreting tumors in the adrenal medulla can lead to very high levels of circulating catecholamines (both epinephrine and norepinephrine). This leads to alpha-adrenoceptor mediated systemic vasoconstriction and beta-adrenoceptor mediated cardiac stimulation, both of which contribute to significant elevations in arterial pressure. […] This is a serious condition that sometimes develops during the third trimester of pregnancy that causes hypertension due to increased blood volume, which increases cardiac output by the Frank-Starling mechanism. […] Obstruction of the aorta at this point reduces distal arterial pressures and elevates arterial pressures in the head and arms. The reduced systemic arterial pressure activates the renin-angiotensin-aldosterone system, which leads to an increase in blood volume, which further increases arterial pressures in the upper body and may largely offset the reduction in lower body arterial pressures.

• #85 Diagnosing Secondary Hypertension | AAFP

  https://www.aafp.org/pubs/afp/issues/2003/0101/p67.html

  Obstructive sleep apnea (OSA), a repetitive mechanical obstruction of the upper airway during sleep, is an independent risk factor for hypertension. […] Primary hyperaldosteronism is defined as overproduction of aldosterone independent of its usual regulator, the renin-angiotensin system. […] Renovascular hypertension is defined as hypertension resulting from compromised arterial supply to the kidneys. […] Renal parenchymal disease can be a cause or consequence of hypertension. […] Excess catecholamine levels play a role in causing white-coat hypertension and hypertension in pheochromocytoma, OSA, and other diseases discussed in this article. […] Coarctation of the aorta is a congenital narrowing of the aortic lumen, most often occurring just distal to the origin of the left subclavian artery.

• #86 CV Physiology | Secondary Hypertension

  https://cvphysiology.com/blood-pressure/bp023

  Pathologic processes (e.g., diabetic nephropathy, glomerulonephritis) can damage nephrons in the kidney. When this occurs, the kidney cannot excrete normal amounts of sodium, which leads to sodium and water retention, increased blood volume, and increased cardiac output by the Frank-Starling mechanism. […] Increased circulating aldosterone causes renal retention of sodium and water, which causes blood volume and arterial pressure to increase. […] Emotional stress leads to activation of the sympathetic nervous system, which causes increased release of norepinephrine from sympathetic nerves in the heart and blood vessels, leading to increased cardiac output and increased systemic vascular resistance. […] The mechanism of hypertension may be related to sympathetic activation and hormonal changes associated with repeated periods of apnea-induced hypoxia and hypercapnia, and from stress associated with the loss of sleep.

• #87 CV Physiology | Secondary Hypertension

  https://cvphysiology.com/blood-pressure/bp023

  Pathologic processes (e.g., diabetic nephropathy, glomerulonephritis) can damage nephrons in the kidney. When this occurs, the kidney cannot excrete normal amounts of sodium, which leads to sodium and water retention, increased blood volume, and increased cardiac output by the Frank-Starling mechanism. […] Increased circulating aldosterone causes renal retention of sodium and water, which causes blood volume and arterial pressure to increase. […] Emotional stress leads to activation of the sympathetic nervous system, which causes increased release of norepinephrine from sympathetic nerves in the heart and blood vessels, leading to increased cardiac output and increased systemic vascular resistance. […] The mechanism of hypertension may be related to sympathetic activation and hormonal changes associated with repeated periods of apnea-induced hypoxia and hypercapnia, and from stress associated with the loss of sleep.

• #88 Diagnosing Secondary Hypertension | AAFP

  https://www.aafp.org/pubs/afp/issues/2003/0101/p67.html

  Obstructive sleep apnea (OSA), a repetitive mechanical obstruction of the upper airway during sleep, is an independent risk factor for hypertension. […] Primary hyperaldosteronism is defined as overproduction of aldosterone independent of its usual regulator, the renin-angiotensin system. […] Renovascular hypertension is defined as hypertension resulting from compromised arterial supply to the kidneys. […] Renal parenchymal disease can be a cause or consequence of hypertension. […] Excess catecholamine levels play a role in causing white-coat hypertension and hypertension in pheochromocytoma, OSA, and other diseases discussed in this article. […] Coarctation of the aorta is a congenital narrowing of the aortic lumen, most often occurring just distal to the origin of the left subclavian artery.

• #89 CV Physiology | Secondary Hypertension

  https://cvphysiology.com/blood-pressure/bp023

  Elevated thyroxin levels cause increased blood volume through activation of the renin-angiotensin-aldosterone system, and increased heart rate and ventricular contractility. […] Catecholamine secreting tumors in the adrenal medulla can lead to very high levels of circulating catecholamines (both epinephrine and norepinephrine). This leads to alpha-adrenoceptor mediated systemic vasoconstriction and beta-adrenoceptor mediated cardiac stimulation, both of which contribute to significant elevations in arterial pressure. […] This is a serious condition that sometimes develops during the third trimester of pregnancy that causes hypertension due to increased blood volume, which increases cardiac output by the Frank-Starling mechanism. […] Obstruction of the aorta at this point reduces distal arterial pressures and elevates arterial pressures in the head and arms. The reduced systemic arterial pressure activates the renin-angiotensin-aldosterone system, which leads to an increase in blood volume, which further increases arterial pressures in the upper body and may largely offset the reduction in lower body arterial pressures.

• #90 Diagnosing Secondary Hypertension | AAFP

  https://www.aafp.org/pubs/afp/issues/2003/0101/p67.html

  Cushing’s syndrome can cause hypertension via the mineralocorticoid effects of excess glucocorticoids and is best screened for with a dexamethasone-suppression test. […] Many prescription and nonprescription drugs can cause or exacerbate hypertension. […] Excess consumption of dietary sodium is linked to chronic hypertension, although the lower limit of excess can be difficult to define. […] Elevated erythropoietin levels can be endogenous (as in response to the chronic hypoxia of COPD) or exogenous (administered to alleviate the anemia seen in chronic renal failure). […] Hypothyroidism can cause decreased cardiac output with a compensatory increase in vascular tone, resulting in a more prominent rise in diastolic blood pressure than in systolic blood pressure. […] Hyperparathyroidism (primary or secondary to chronic renal insufficiency) is a potentially reversible cause of hypertension. […] Pheochromocytoma is another endocrine cause of hypertension. […] Acromegaly (elevated growth hormone) is a rare endocrine cause of hypertension.

• #91 Drug-Induced Hypertension

  https://www.uspharmacist.com/article/drug-induced-hypertension

  Drug-induced blood pressure elevations represent an important and modifiable cause of secondary hypertension; therefore, it is imperative that pharmacists recognize this causal relationship. […] It is well established that sympathomimetic amines cause dose-related increases in blood pressure. […] Sympathomimetic-induced hypertension may not be clinically significant in healthy patients, but it can become hazardous in others. […] Drug-induced hypertension associated with NSAIDs is due to the renal effects of these drugs. […] Specifically, NSAIDs cause dose-related increases in sodium and water retention. […] The principal mechanism of corticosteroid-induced hypertension is the overstimulation of the mineralocorticoid receptor, resulting in sodium retention in the kidney. […] Corticosteroid-induced fluid retention can be severe enough to cause hypertension, and patients with preexisting hypertension may develop a worsening of blood pressure control when these drugs are initiated.

• #92 Drug-Induced Hypertension

  https://www.uspharmacist.com/article/drug-induced-hypertension

  The likely mechanism of venlafaxine-induced hypertension is the increase in levels of norepinephrine and the subsequent potentiation of noradrenergic neurotransmission. […] The clinical significance of sibutramine-induced hypertension is not well defined. […] The exact mechanism of cyclosporine-induced hypertension is uncertain, but several hypotheses have been proposed, including increased prostaglandin synthesis and decreased water, sodium, and potassium excretion. […] The mechanism of tacrolimus-induced hypertension is postulated to be similar to cyclosporine’s. […] Pharmacists should maintain an awareness of the major drug classes that may increase blood pressure and/or interfere with effective blood pressure control.

• #93 Drug-Induced Hypertension

  https://www.uspharmacist.com/article/drug-induced-hypertension

  The likely mechanism of venlafaxine-induced hypertension is the increase in levels of norepinephrine and the subsequent potentiation of noradrenergic neurotransmission. […] The clinical significance of sibutramine-induced hypertension is not well defined. […] The exact mechanism of cyclosporine-induced hypertension is uncertain, but several hypotheses have been proposed, including increased prostaglandin synthesis and decreased water, sodium, and potassium excretion. […] The mechanism of tacrolimus-induced hypertension is postulated to be similar to cyclosporine’s. […] Pharmacists should maintain an awareness of the major drug classes that may increase blood pressure and/or interfere with effective blood pressure control.

• #94 Pathophysiology of Hypertension: Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension

  https://emedicine.medscape.com/article/1937383-overview

  The pathogenesis of essential hypertension (primary hypertension, idiopathic hypertension) is multifactorial and highly complex, often involving reciprocal influences between different cardiovascular control systems. […] The kidney is both the contributing and the target organ of the hypertensive processes, and the disease involves the interaction of multiple organ systems and numerous mechanisms of independent or interdependent pathways. Factors that play an important role in the pathogenesis of hypertension include the aging process, genetics, activation of neurohormonal systems such as the sympathetic nervous system and renin-angiotensin-aldosterone system, obesity, gut microbiome, and increased dietary salt intake. […] The hallmark hemodynamic anomaly that is key to elevated blood pressure (BP) is an increase of systemic vascular resistance, caused by altered cardiovascular regulatory systems (such as through genetic and environmental factors).

• #95 Hypertension in the African American population: A succinct look at its epidemiology, pathogenesis, and therapy | Nefrología

  https://www.revistanefrologia.com/es-hypertension-in-african-american-population-articulo-S0211699515000260

  Arterial hypertension is prevalent in the black population in the United States. It is directly related to cardiovascular and kidney damage. Its pathogenesis is complex and includes the high incidence of obesity, salt sensitivity and the activation of the renin-angiotensinaldosterone system. […] The pathogenesis involves multiple mechanisms with the interaction of different factors like obesity, salt sensitivity, renin angiotensin system, and endothelium vascular response among others. […] There are several pathophysiological mechanisms linked to the development of HTN and are disproportionately prevalent in selected racial/ethnic groups like AA. […] Obesity contributes significantly to HTN in all populations. Is more prevalent in both AA and Hispanics, particularly in women, compared with whites.

• #96 Advances in pathogenesis and treatment of essential hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9616110/

  Sympathetic dysregulation is also an important cause of essential hypertension. […] The sympathetic overdrive leads to increased cardiac output, increased systemic vascular tone, and elevated plasma catecholamine levels. […] The interplay of these factors leads to a net-like pathogenesis of essential hypertension and increases the difficulty of the treatment. […] In our opinion, the pathogenesis of hypertension is based on both decreased vasodilation and increased blood volume.

• #97 Advances in pathogenesis and treatment of essential hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9616110/

  Sympathetic dysregulation is also an important cause of essential hypertension. […] The sympathetic overdrive leads to increased cardiac output, increased systemic vascular tone, and elevated plasma catecholamine levels. […] The interplay of these factors leads to a net-like pathogenesis of essential hypertension and increases the difficulty of the treatment. […] In our opinion, the pathogenesis of hypertension is based on both decreased vasodilation and increased blood volume.

• #98 Hypertension: pathophysiology and diagnosis – The Pharmaceutical Journal

  https://pharmaceutical-journal.com/article/ld/hypertension-pathophysiology-and-diagnosis

  Hypertension, or high blood pressure, is the leading risk factor associated with death in the world but is largely asymptomatic and often undetected in patients. […] Hypertension is typically asymptomatic and only detected through opportunistic screening. Symptoms only manifest when blood pressure reaches very high levels (usually >200 mmHg systolic), and can include headaches, dizziness and nosebleeds. […] Hypertension is one of the most important preventable causes of premature morbidity and mortality, and lowering blood pressure reduces the risk of cardiovascular events in people with established hypertension. Each 2 mmHg rise in systolic blood pressure is associated with a 7% increased risk of death from coronary heart disease and a 10% increased risk of death from stroke. […] Blood pressure is determined by the cardiac output balanced against systemic vascular resistance. The process of maintaining blood pressure is complex, and involves numerous physiological mechanisms, including arterial baroreceptors, the renin–angiotensin–aldosterone system, atrial natriuretic peptide, endothelins, and mineralocorticoid and glucocorticoid steroids. Together, these complex systems manage the degree of vasodilatation or vasoconstriction within the systemic circulation, and the retention or excretion of sodium and water, to maintain an adequate circulating blood volume.

• #99 Hypertension: pathophysiology and diagnosis – The Pharmaceutical Journal

  https://pharmaceutical-journal.com/article/ld/hypertension-pathophysiology-and-diagnosis

  Hypertension, or high blood pressure, is the leading risk factor associated with death in the world but is largely asymptomatic and often undetected in patients. […] Hypertension is typically asymptomatic and only detected through opportunistic screening. Symptoms only manifest when blood pressure reaches very high levels (usually >200 mmHg systolic), and can include headaches, dizziness and nosebleeds. […] Hypertension is one of the most important preventable causes of premature morbidity and mortality, and lowering blood pressure reduces the risk of cardiovascular events in people with established hypertension. Each 2 mmHg rise in systolic blood pressure is associated with a 7% increased risk of death from coronary heart disease and a 10% increased risk of death from stroke. […] Blood pressure is determined by the cardiac output balanced against systemic vascular resistance. The process of maintaining blood pressure is complex, and involves numerous physiological mechanisms, including arterial baroreceptors, the renin–angiotensin–aldosterone system, atrial natriuretic peptide, endothelins, and mineralocorticoid and glucocorticoid steroids. Together, these complex systems manage the degree of vasodilatation or vasoconstriction within the systemic circulation, and the retention or excretion of sodium and water, to maintain an adequate circulating blood volume.

• #100 Hypertension: pathophysiology and diagnosis – The Pharmaceutical Journal

  https://pharmaceutical-journal.com/article/ld/hypertension-pathophysiology-and-diagnosis

  Dysfunction in any of these processes can lead to the development of hypertension. This may be through increased cardiac output, increased systemic vascular resistance, or both. […] No specific cause of hypertension is found for most (>95%) patients with high blood pressure, and this is often referred to as primary or essential hypertension. Secondary causes are identified in the remaining 5% of cases. […] Patients with suspected secondary hypertension should be referred to a specialist team. […] Hypertension is not a disease in its own right, but if left untreated it is a risk factor for acute events (such as myocardial infarction and stroke) and for the development of organ damage. […] Chronically raised blood pressure can lead to several conditions related to pressure overload: left ventricular hypertrophy, which is the result of chronic pressure overload in the myocardium, resulting in thickening of the muscle; this slows ventricular relaxation and delays filling during diastole, reducing the efficiency of the heart as a pump.

• #101 Decoding the mechanism of hypertension through multiomics profiling | Journal of Human Hypertension

  https://www.nature.com/articles/s41371-022-00769-8

  Hypertension, characterised by a constant high blood pressure, is the primary risk factor for multiple cardiovascular events and a major cause of death in adults. […] High blood pressure results from the interplay between genetic and environmental factors. […] Hypertension is the consequence of the interaction of vascular cells such as endothelial cells and arterial smooth muscle cells. […] The multifactorial and asymptomatic nature of hypertension complicates its detection, and prediction of those who are likely to develop the condition is uncertain. […] The reasons for poor blood pressure control include medication side effects, poor patient provider relationship, non-adherence to medications, obesity, family history and the presence of comorbidity. […] Baroreflex through the action of stretch receptors on carotid sinus and aorta, provides a negative feedback loop that regulate blood pressure.

• #102 Pathophysiology of Hypertension: Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension

  https://emedicine.medscape.com/article/1937383-overview

  The pathogenesis of essential hypertension (primary hypertension, idiopathic hypertension) is multifactorial and highly complex, often involving reciprocal influences between different cardiovascular control systems. […] The kidney is both the contributing and the target organ of the hypertensive processes, and the disease involves the interaction of multiple organ systems and numerous mechanisms of independent or interdependent pathways. Factors that play an important role in the pathogenesis of hypertension include the aging process, genetics, activation of neurohormonal systems such as the sympathetic nervous system and renin-angiotensin-aldosterone system, obesity, gut microbiome, and increased dietary salt intake. […] The hallmark hemodynamic anomaly that is key to elevated blood pressure (BP) is an increase of systemic vascular resistance, caused by altered cardiovascular regulatory systems (such as through genetic and environmental factors).

• #103 High Blood Pressure – Heart and Blood Vessel Disorders – Merck Manual Consumer Version

  https://www.merckmanuals.com/home/heart-and-blood-vessel-disorders/high-blood-pressure/high-blood-pressure

  High blood pressure (hypertension) is persistently high pressure in the arteries. […] Often no cause for high blood pressure can be identified, but sometimes it occurs as a result of an underlying disorder of the kidneys or a hormonal disorder. […] Obesity, a sedentary lifestyle, stress, smoking, and excessive amounts of alcohol or sodium (salt) in the diet all can play a role in the development of high blood pressure in people who have an inherited tendency to develop it. […] Changes due to aging may contribute to high blood pressure with no known cause (primary hypertension). As people age, large arteries gradually stiffen and small arteries may become partially blocked. Some experts think that this stiffening, combined with the narrowing of small arteries, may partly explain why blood pressure increases as people age.

• #104 The pathophysiology of hypertension

  https://pmc.ncbi.nlm.nih.gov/articles/PMC1120075/

  Epidemiologically there is a clustering of several risk factors, including obesity, hypertension, glucose intolerance, diabetes mellitus, and hyperlipidaemia. […] Although separate genes and genetic factors have been linked to the development of essential hypertension, multiple genes are most likely contribute to the development of the disorder in a particular individual. […] Some specific genetic mutations can rarely cause hypertension. Experimental models of genetic hypertension have shown that the inherited tendency to hypertension resides primarily in the kidney. […] There is increasing evidence that fetal influences, particularly birth weight, may be a determinant of blood pressure in adult life.

• #105 Hypertension in the African American population: A succinct look at its epidemiology, pathogenesis, and therapy | Nefrología

  https://www.revistanefrologia.com/es-hypertension-in-african-american-population-articulo-S0211699515000260

  Arterial hypertension is prevalent in the black population in the United States. It is directly related to cardiovascular and kidney damage. Its pathogenesis is complex and includes the high incidence of obesity, salt sensitivity and the activation of the renin-angiotensinaldosterone system. […] The pathogenesis involves multiple mechanisms with the interaction of different factors like obesity, salt sensitivity, renin angiotensin system, and endothelium vascular response among others. […] There are several pathophysiological mechanisms linked to the development of HTN and are disproportionately prevalent in selected racial/ethnic groups like AA. […] Obesity contributes significantly to HTN in all populations. Is more prevalent in both AA and Hispanics, particularly in women, compared with whites.

• #106 Hypertension in the African American population: A succinct look at its epidemiology, pathogenesis, and therapy | Nefrología

  https://www.revistanefrologia.com/es-hypertension-in-african-american-population-articulo-S0211699515000260

  Salt sensitivity is prevalent in AA, particularly those with HTN. […] The role of the renin-angiotensin system (RAAS) in AA has not been clearly defined but the pattern of excessive RAAS dependent target-organ injury (LVH, CKD/proteinuria) in AA, showcases the importance of the RAAS in this population. […] Obesity, salt sensitivity, RAAS, and endothelial activation represent different factors affecting the pathogenesis of HTN. The understanding of how this factors influence BP will guide the development of treatment protocols that will optimize the way we implement diet, physical activity and drug therapy. […] The cardiovascular and renal consequences of HTN are greater in blacks, relative to their white counterparts. Structural vascular abnormalities as well as genetic, geographic, and environmental factors may play an important role.

• #107 Hypertension – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/hypertension/hypertension

  Hypertension may be […] Primary (no specific cause85% of cases) […] Secondary (an identified cause) […] Hemodynamics and physiologic components (eg, plasma volume, activity of the renin-angiotensin system) vary, indicating that primary hypertension is unlikely to have a single cause. Even if one factor is recognized, multiple factors are probably involved in sustaining elevated blood pressure (the mosaic theory). Heredity is a predisposing factor, but the exact mechanism by which genetics plays a role is unclear. At younger ages, environmental factors (eg, dietary sodium, stress) seem to affect only people who are genetically susceptible; however, in patients 65 years, high sodium intake becomes more likely to precipitate hypertension. […] Because blood pressure equals cardiac output (CO) multiplied by total peripheral vascular resistance (TPR), pathogenic mechanisms involve

• #108 Genetic Factors Contributing to the Pathogenesis of Essential Hypertension in Two African Populations

  https://www.mdpi.com/2075-4426/14/3/323

  The Sodium Retention Hypothesis suggests that, evolutionarily, the capacity to retain salt provided a biological advantage and increased the fitness of salt retainers in tropical hunter-gatherer societies. […] Our investigation identified significant associations between EH and five variants in genes related to the renin–angiotensin–aldosterone system (RAAS): CYP11B2 rs179998, AGT rs5051, AGT rs699, AGTR1 rs5186, and ACE rs4646994. […] The observed associations between RAAS variants and EH in our study support the Sodium Retention Hypothesis and highlight the need for pharmacogenetic research of anti-hypertensive treatment in these population groups. […] The ACE gene’s rs4646994 variant, an insertion/deletion polymorphism, unveiled opposing associations with EH, echoing the complex nature of genetic influences on BP regulation.

• #109 Hypertension – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/hypertension/hypertension

  Hypertension may be […] Primary (no specific cause85% of cases) […] Secondary (an identified cause) […] Hemodynamics and physiologic components (eg, plasma volume, activity of the renin-angiotensin system) vary, indicating that primary hypertension is unlikely to have a single cause. Even if one factor is recognized, multiple factors are probably involved in sustaining elevated blood pressure (the mosaic theory). Heredity is a predisposing factor, but the exact mechanism by which genetics plays a role is unclear. At younger ages, environmental factors (eg, dietary sodium, stress) seem to affect only people who are genetically susceptible; however, in patients 65 years, high sodium intake becomes more likely to precipitate hypertension. […] Because blood pressure equals cardiac output (CO) multiplied by total peripheral vascular resistance (TPR), pathogenic mechanisms involve

• #110 Hypertension – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/hypertension/hypertension

  Hypertension may be […] Primary (no specific cause85% of cases) […] Secondary (an identified cause) […] Hemodynamics and physiologic components (eg, plasma volume, activity of the renin-angiotensin system) vary, indicating that primary hypertension is unlikely to have a single cause. Even if one factor is recognized, multiple factors are probably involved in sustaining elevated blood pressure (the mosaic theory). Heredity is a predisposing factor, but the exact mechanism by which genetics plays a role is unclear. At younger ages, environmental factors (eg, dietary sodium, stress) seem to affect only people who are genetically susceptible; however, in patients 65 years, high sodium intake becomes more likely to precipitate hypertension. […] Because blood pressure equals cardiac output (CO) multiplied by total peripheral vascular resistance (TPR), pathogenic mechanisms involve

• #111 Hypertension – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/hypertension/hypertension

  Hypertension may be […] Primary (no specific cause85% of cases) […] Secondary (an identified cause) […] Hemodynamics and physiologic components (eg, plasma volume, activity of the renin-angiotensin system) vary, indicating that primary hypertension is unlikely to have a single cause. Even if one factor is recognized, multiple factors are probably involved in sustaining elevated blood pressure (the mosaic theory). Heredity is a predisposing factor, but the exact mechanism by which genetics plays a role is unclear. At younger ages, environmental factors (eg, dietary sodium, stress) seem to affect only people who are genetically susceptible; however, in patients 65 years, high sodium intake becomes more likely to precipitate hypertension. […] Because blood pressure equals cardiac output (CO) multiplied by total peripheral vascular resistance (TPR), pathogenic mechanisms involve

• #112 Hypertension – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/hypertension/hypertension

  Increased CO […] Increased TPR […] Both […] In most patients with hypertension, CO is normal or slightly increased, and TPR is increased. This pattern is typical of primary hypertension and hypertension due to primary aldosteronism, pheochromocytoma, renovascular disease, and renal parenchymal disease. […] In many cases of hypertension, sodium transport across the vascular cell membrane is abnormal, because the sodium-potassium pump (Na+, K+-ATPase) is defective or inhibited, or because permeability to sodium ions is increased. The result is increased intracellular sodium and calcium, which makes the cell more sensitive to sympathetic stimulation. […] Sympathetic stimulation increases blood pressure, usually more in patients with hypertension than in patients who are normotensive.

• #113 Pathophysiology of Hypertension: Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension

  https://emedicine.medscape.com/article/1937383-overview

  The pathogenesis of essential hypertension (primary hypertension, idiopathic hypertension) is multifactorial and highly complex, often involving reciprocal influences between different cardiovascular control systems. […] The kidney is both the contributing and the target organ of the hypertensive processes, and the disease involves the interaction of multiple organ systems and numerous mechanisms of independent or interdependent pathways. Factors that play an important role in the pathogenesis of hypertension include the aging process, genetics, activation of neurohormonal systems such as the sympathetic nervous system and renin-angiotensin-aldosterone system, obesity, gut microbiome, and increased dietary salt intake. […] The hallmark hemodynamic anomaly that is key to elevated blood pressure (BP) is an increase of systemic vascular resistance, caused by altered cardiovascular regulatory systems (such as through genetic and environmental factors).

• #114 Hypertension in the African American population: A succinct look at its epidemiology, pathogenesis, and therapy | Nefrología

  https://www.revistanefrologia.com/es-hypertension-in-african-american-population-articulo-S0211699515000260

  Salt sensitivity is prevalent in AA, particularly those with HTN. […] The role of the renin-angiotensin system (RAAS) in AA has not been clearly defined but the pattern of excessive RAAS dependent target-organ injury (LVH, CKD/proteinuria) in AA, showcases the importance of the RAAS in this population. […] Obesity, salt sensitivity, RAAS, and endothelial activation represent different factors affecting the pathogenesis of HTN. The understanding of how this factors influence BP will guide the development of treatment protocols that will optimize the way we implement diet, physical activity and drug therapy. […] The cardiovascular and renal consequences of HTN are greater in blacks, relative to their white counterparts. Structural vascular abnormalities as well as genetic, geographic, and environmental factors may play an important role.

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