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 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). […] Over time, chronic elevated BP modifies structures of the heart and large and small arteries, which in turn promote hypertension. […] 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.

• #2 Essential Hypertension – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK539859/

  The current definition of hypertension (HTN) is systolic blood pressure (SBP) values of 130 mm Hg or more and/or diastolic blood pressure (DBP) of more than 80 mm Hg. Hypertension ranks among the most common chronic medical condition characterized by a persistent elevation in arterial pressure. […] Most cases of hypertension are idiopathic, which is also known as essential hypertension. It has long been suggested that an increase in salt intake increases the risk of developing hypertension. One of the described factors for the development of essential hypertension is the patient’s genetic ability to salt response. About 50% to 60% of the patients are salt sensitive and therefore tend to develop hypertension. […] There are various mechanisms described for the development of hypertension, which include increased salt absorption resulting in volume expansion, an impaired response of the renin-angiotensin-aldosterone system (RAAS), and increased activation of the sympathetic nervous system. These changes lead to the development of increased total peripheral resistance and increased afterload, which in turn leads to the development of hypertension.

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

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

  Hypertension is defined as a systolic blood pressure (BP) 130 mm Hg or a diastolic blood pressure 80 mm Hg or taking medication for hypertension. […] 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). […] Because blood pressure equals cardiac output (CO) multiplied by total peripheral vascular resistance (TPR), pathogenic mechanisms involve increased CO, increased TPR, or 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.

• #4 Pathophysiology of Hypertension | SpringerLink

  https://link.springer.com/doi/10.1007/978-3-540-76341-3_61

  Blood pressure can fundamentally be viewed as a function of cardiac output (CO) and systemic vascular resistance. […] Recent research has begun to unravel relationships at the cellular and molecular levels that exert important effects on blood pressure. […] The endothelium, intima, vascular smooth muscle and extracellular matrix interact with each other and with vasomotor, growth factors, transcriptional, hormonal and neuronal factors that affect signal transduction, gene transcription, ion transport, tissue remodeling and cellular response, all in the context of the patients genetic background.

• #5 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.

• #6 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. […] An inflammatory process often accompanies hypertension. […] It has been suggested that a common molecular basis that connects immunoinflammation to hypertension is oxidative stress and increased generation of reactive oxygen species.

• #7 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.

• #8 Hypertension: Practice Essentials, Background, Pathophysiology

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

  In this situation, cardiac output is generally normal or slightly reduced, and circulating blood volume is normal. […] 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. […] Sympathetic nervous system activation and noradrenergic stimuli have also been shown to promote T-lymphocyte activation and infiltration, and contribute to the pathophysiology of hypertension.

• #9 Advances in pathogenesis and treatment of essential hypertension

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

  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. […] 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.

• #10 Pathophysiology of hypertension – Wikipedia

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

  Another system maintaining the extracellular fluid volume, peripheral resistance, and that if disturbed may lead to hypertension, is the reninangiotensinaldosterone 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 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.

• #10 Pathophysiology of hypertension – Wikipedia

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

  Exposure to stress increases sympathetic outflow, and repeated stress-induced vasoconstriction may result in vascular hypertrophy, leading to progressive increases in peripheral resistance and blood pressure. This could partly explain the greater incidence of hypertension in lower socioeconomic groups, since they must endure greater levels of stress associated with daily living. Persons with a family history of hypertension manifest augmented vasoconstrictor and sympathetic responses to laboratory stressors, such as cold pressor testing and mental stress, that may predispose them to hypertension. This is particularly true of young African Americans. Exaggerated stress responses may contribute to the increased incidence of hypertension in this group. For patients having hypertension, higher heart rate variability (HRV) is a risk factor for atrial fibrillation.

• #10 Pathophysiology of hypertension – Wikipedia

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

  The endothelium of blood vessels produces an extensive range of substances that influence blood flow and, in turn, is affected by changes in the blood and the pressure of blood flow. For example, local nitric oxide and endothelin, which are secreted by the endothelium, are the major regulators of vascular tone and blood pressure. In patients with essential hypertension, the balance between the vasodilators and the vasoconstrictors is upset, which leads to changes in the endothelium and sets up a „vicious cycle” that contributes to the maintenance of high blood pressure. In patients with hypertension, endothelial activation and damage also lead to changes in vascular tone, vascular reactivity, and coagulation and fibrinolytic pathways. Alterations in endothelial function are a reliable indicator of target organ damage and atherosclerotic disease, as well as prognosis.

• #10 Pathophysiology of hypertension – Wikipedia

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

  A 2007 review article states that while excessive sodium consumption has long been recognized as contributing to the risk of hypertension, „potassium, the main intracellular cation, has usually been viewed as a minor factor in the pathogenesis of hypertension. However, abundant evidence indicates that a potassium deficit has a critical role in hypertension and its cardiovascular sequelae.” The authors state that modern, western, high sodium, low potassium diets result in corresponding changes in intracellular concentration of these, the two most important cations in animal cells. This imbalance leads to contraction of vascular smooth muscle, restricting blood flow and so driving up blood pressure. The authors cite studies which show that potassium supplementation is effective in reducing hypertension.

• #10 Pathophysiology of hypertension – Wikipedia

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

  Epidemiological support for this hypothesis can be found in a 2014 meta-analysis which states that „the sodium-to-potassium ratio appears to be more strongly associated with blood pressure outcomes than either sodium or potassium alone in hypertensive adult populations.” […] Basic science discoveries have implicated the immune system as in the development of hypertension in animal models. Population studies in humans have reported that higher levels of certain inflammatory cytokines are associated with greater risk of hypertension development.

• #11 Homeostatic Regulation of the Vascular System | Anatomy and Physiology II

  https://courses.lumenlearning.com/suny-ap2/chapter/homeostatic-regulation-of-the-vascular-system/

  The renin-angiotensin-aldosterone mechanism has a major effect upon the cardiovascular system. Renin is an enzyme, although because of its importance in the renin-angiotensin-aldosterone pathway, some sources identify it as a hormone. Specialized cells in the kidneys found in the juxtaglomerular apparatus respond to decreased blood flow by secreting renin into the blood. Renin converts the plasma protein angiotensinogen, which is produced by the liver, into its active form angiotensin I. Angiotensin I circulates in the blood and is then converted into angiotensin II in the lungs. This reaction is catalyzed by the enzyme angiotensin-converting enzyme (ACE). Angiotensin II is a powerful vasoconstrictor, greatly increasing blood pressure. It also stimulates the release of ADH and aldosterone, a hormone produced by the adrenal cortex. Aldosterone increases the reabsorption of sodium into the blood by the kidneys. Since water follows sodium, this increases the reabsorption of water. This in turn increases blood volume, raising blood pressure.

• #12 Mechanisms of obesity-induced hypertension | Hypertension Research

  https://www.nature.com/articles/hr20109

  Activation of the sympathetic nervous system (SNS), measured with direct or indirect methods, has been considered to have a crucial function in the pathogenesis of hypertension among obese individuals. […] The mechanisms that have been proposed to be responsible for an increased sympathetic activity in obesity include impaired function of the baroreceptor sensitivity, increased levels of circulating free-fatty acids (FFAs), angiotensin (Ang) II, insulin and leptin. […] The arterial pressure control mechanism of diuresis and natriuresis according to the principle of infinite feedback gain seems to be shifted toward higher BP values in obese patients. […] Several studies have shown predominantly high levels of plasma renin activity, plasma angiotensinogen, Ang II and aldosterone values in association with human obesity.

• #13 Hypertension: What Causes High Blood Pressure and How to Treat It > News > Yale Medicine

  https://www.yalemedicine.org/news/what-causes-high-blood-pressure

  But 48% of Americans have high blood pressure, also known as hypertension, and managing the condition is important because untreated hypertension increases the risk of stroke, vascular dementia, heart attack, and congestive heart failure, among other problems, says Erica Spatz, MD, MHS, director of the Yale Medicine Preventive Cardiovascular Health Program. […] High blood pressure increases in prevalence with age, and genetics also play a role, Dr. Spatz says. Other factors that contribute to hypertension include sleep, stress, diet, physical activity, and psychological factors, such as a history of depression or anxiety, loneliness, and discrimination, adds Allison Gaffey, PhD, a Yale Medicine psychologist who specializes in cardiology. Over time, chronic stress can elevate your hormone levels, including the hormone cortisol, which raises blood pressure, Gaffey explains. […] High blood pressure, or hypertension, is a condition that increases the force of blood against the artery walls. Learn about symptoms and treatment.

• #14 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. […] Hypertension is a complex condition and understanding its pathophysiology has implications for treatment and delay of complications.

• #15 Advances in pathogenesis and treatment of essential hypertension

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

  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. […] 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.

• #16 CV Physiology | Secondary Hypertension

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

  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). […] Therefore, hypertension caused by renal artery stenosis results from both an increase in systemic vascular resistance and an increase in cardiac output. […] The elevation in arterial pressure secondary to renal disease can be viewed as an attempt by the kidney to increase renal perfusion and restore glomerular filtration.

• #17 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. […] 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. […] Obstructive sleep apnea (OSA), a repetitive mechanical obstruction of the upper airway during sleep, is an independent risk factor for hypertension.

• #18 Diagnosing Secondary Hypertension | AAFP

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

  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. […] Cushing’s syndrome can cause hypertension via the mineralocorticoid effects of excess glucocorticoids and is best screened for with a dexamethasone-suppression test.

• #19 Diagnosing Secondary Hypertension | AAFP

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

  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.

• #20 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, 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. […] By inhibiting COX-2’s natriuretic effect, thereby increasing sodium retention, all NSAIDs carry with them the consequent risk of increased fluid retention. […] The principal mechanism of corticosteroid-induced hypertension is the overstimulation of the mineralocorticoid receptor, resulting in sodium retention in the kidney. This results in volume expansion and a subsequent increase in blood pressure.

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

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

  Deficiency of a vasodilator (eg, bradykinin, nitric oxide), rather than excess of a vasoconstrictor (eg, angiotensin, norepinephrine), may cause 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), renal failure, and death. […] Elevated BP levels lead to the development of generalized arteriolosclerosis and acceleration of atherogenesis. […] Because afterload is increased in patients with elevated BP, the left ventricle gradually hypertrophies, causing diastolic dysfunction. […] The higher the blood pressure, and the more severe the retinal changes and other evidence of target-organ involvement, the worse the prognosis.

• #22 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. […] 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.

• #23 What is High Blood Pressure? | American Heart Association

  https://www.heart.org/en/health-topics/high-blood-pressure/the-facts-about-high-blood-pressure

  High blood pressure is also known as hypertension. It happens when the force of your blood pushing against the walls of your blood vessels is too high. High blood pressure can lead to other serious problems such as heart attack and stroke. […] When blood pressure is high for too long, it can damage the walls of blood vessels, causing them to develop tiny tears. To fix these damaged areas, the body sends special cells that stick to the site. Over time, substances such as cholesterol and fats may also build up at these damaged spots, forming plaque. […] As plaque slowly builds, a process called atherosclerosis, it can make the inside of the arteries narrower. This narrowing can block the flow of blood, further increasing blood pressure. […] It’s important to recheck your blood pressure with your health care team. They can confirm if this reading is within your target blood pressure range and discuss any steps you might need to take to keep it in a healthy range. Lifestyle changes can help.

• #24 How High Blood Pressure Can Lead to a Heart Attack | American Heart Association

  https://www.heart.org/en/health-topics/high-blood-pressure/health-threats-from-high-blood-pressure/how-high-blood-pressure-can-lead-to-a-heart-attack

  When blood pressure is high for too long, it can damage the walls of blood vessels, causing them to develop tiny tears. […] Over time, substances like cholesterol and fats may also build up at these damaged spots, forming plaque. […] As plaque slowly builds, a process called atherosclerosis, it can make the inside of the arteries narrower and block the flow of blood to the heart. […] Blood flow can also become blocked if the plaque ruptures or breaks off and forms a clot. […] When blood flow is blocked (by either plaque buildup or a clot), that part of the heart doesn’t get the oxygen and nutrients it needs.

• #25 Advances in pathogenesis and treatment of essential hypertension

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

  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. […] As a congenital factor, genes can simultaneously affect RAAS, water-sodium retention, arterial stiffness, and sympathetic nerves.

• #26 Mechanisms of obesity-induced hypertension | Hypertension Research

  https://www.nature.com/articles/hr20109

  Insulin resistance, low levels of adiponectin, high plasma leptin, increased levels of plasma glucose and FFAs are considered as indices of an inflammation compatible profile. […] Long-term sympathetic and RAS activation leads to small artery vasoconstriction and remodeling, which increases wall to lumen ratio and may act synergistically with large artery damage to raise BP. […] Understanding of the mechanisms associated with obesity-related hypertension is essential for refined treatment strategies.

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