The document summarizes the pathophysiology of arterial hypertension. It describes how blood pressure is regulated through factors like cardiac output, total peripheral resistance, and circulating blood volume. It then discusses the classification, causes, risk factors, clinical signs and symptoms, end-organ damage, and established diseases associated with arterial hypertension. The neurogenic, renal, and local vascular mechanisms involved in blood pressure regulation are also summarized.
The document summarizes the pathophysiology of arterial hypertension. It describes how blood pressure is regulated through factors like cardiac output, total peripheral resistance, and circulating blood volume. It then discusses the classification, causes, risk factors, clinical signs and symptoms, end-organ damage, and established diseases associated with arterial hypertension. The neurogenic, renal, and local vascular mechanisms involved in blood pressure regulation are also summarized.
The document summarizes the pathophysiology of arterial hypertension. It describes how blood pressure is regulated through factors like cardiac output, total peripheral resistance, and circulating blood volume. It then discusses the classification, causes, risk factors, clinical signs and symptoms, end-organ damage, and established diseases associated with arterial hypertension. The neurogenic, renal, and local vascular mechanisms involved in blood pressure regulation are also summarized.
The document summarizes the pathophysiology of arterial hypertension. It describes how blood pressure is regulated through factors like cardiac output, total peripheral resistance, and circulating blood volume. It then discusses the classification, causes, risk factors, clinical signs and symptoms, end-organ damage, and established diseases associated with arterial hypertension. The neurogenic, renal, and local vascular mechanisms involved in blood pressure regulation are also summarized.
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Arterial hypertension
2024 Biophysical model of the blood pressure (BP) regulation
BP
VCB CO TPR
BP = f (CO, TPR, VCB)
• CO – cardiac output • VCB – volume of the circulating blood • TPR – total peripheral resistance Arterial hypertension - systolic blood pressure >140 mmHg or diastolic blood pressure > 90 mmHg AH is a major cause mortality because it is a major risk factor for: - Stroke - heart failure - renal failure - Atherosclerosis - Dementia Classification: 1. Primary (or essential) hypertension 85% - 95% of all human cases (we don’t know underlying conditions) 2. secondary hypertension Systemic blood pressure regulation Systemic regulation - Neurogenic (SNS, PSNS) - Vasopressin - Kidney: RAAS, Na+-uresis, volume blood circulation - Heart: system of Na+uretic peptide (A and B) - Adrenimedullin (powerful vasodilator) - Immune system Local BP regulation Vasoconstiction Vasodilation • Na+uretic peptide (C) • Angiotensin 2 • NO • Endothelin-1 • Bradykinin • Acetylcholine • Serotonin • Adenosine • Thromboxane А2 • Histamine • Prostaglandin F2α • Prostaglandin E2 • Prostacyclin (PGI2) • Leukotrienes • NO • EDHF Neurogenic control
1). Baroreceptors (mechanoRc)
2). Vasomotor center: - the nucleus tractus solitarius in the dorsal medulla (baroreceptors integration) - the rostral part of the ventral medulla (pressor region) - centers in the pons and midbrain. 3). SNS / PSNS activity Kidneys mechanism BP regulation 1. the production of renin - RAAS 2. renal pressure natriuresis mechanism (macula densa) 3. modulate systemic sympathetic tone by generating impulse via renal afferent nerves. Regulation of RAAS activity This apparatus senses: - the renal perfusion pressure - the sodium concentration in the distal tubular fluid (macula densa) - renin release is stimulated by β- and decreased by α-adrenoceptor stimulation. - High angiotensin II concentrations suppress renin secretion via a negative feedback loop. Kallikrein-kinin systems Tissue kallikreins (kininogen - vasoactive peptides). The most important – bradykinin – vasodilation, water and Na+ uresis . Renomedullary vasodepression
• Renomedullary interstitial cells, located mainly in the renal papilla,
secrete an inactive substance medullipin I. This lipid is transformed in the liver into medullipin II. • This substance exerts a prolonged hypotensive effect, possibly by direct vasodilatation, inhibition of sympathetic drive in response to hypotension, and a diuretic action. The Role of the Vasculature in Hypertension It depends on vascular caliber, reactivity, elasticity. 1. vasoconstrictor hormone: Ang II, catecholamines, and vasopressin, 2. Impairment of endothelium – dependent vasodilation - to inhibit NO production and prostacyclin, and endothelium-derived hyperpolarizing factor 3. ↑ endothelin – 1 and thromboxane A2 4. Larger vessels predominantly use NO, whereas smaller arteries and arterioles are also modulated by endothelium-dependent hyperpolarization and vasodilator prostaglandins 5. traverse MEJs (myoendothelial junctions) In normal condition. Elastic large aorta reflect the pressure wave • In the youth: the pulse pressure is relatively low and the waves reflected by the peripheral vasculature and elastic aorta • With ageing, stiffening of the aorta increases the pulse pressure. It is lead to AH, left ventricular afterload, and contributes to left ventricular hypertrophy.. Immune system • cytokine IL-17A (interleukin 17A) produced by a subset of T cells, innate lymphocytes, histiocytes, and renal tubular cells. • IL-17A affects renal tubular handling of sodium and seems to modulate pressure natriuresis • this cytokine stimulates vascular superoxide production, causes inhibitory phosphorylation of the endothelial NOS, and therefore, reduces the caliber of blood vessels. • Over the long term, IL-17A promotes vascular fibrosis and impairs vascular elasticity. • In contrast, regulatory T cells and anti-inflammatory cytokines, such as IL-10, have antihypertensive effects mediated, in part, by counteracting IL-17A. Arterial hypertension Primary (or essential) Secondary hypertension hypertension 1. Renal • 85% - 95% of all human cases 2. Endocrine • we don’t know underlying 3. Hemodynamic conditions 4. Medicines 5. CNS Risk factors modifiable Non - modifiable - Smoking (now or in the past) - Dyslipidemia - Male sex - Total cholesterol >190 mg/dL and/or HDL- cholesterol ♂<40 mg/dL; ♀<46 mg/dL and/or - Age (♂≥ 55 years; ♀≥ 65 years) - Fasting blood glucose 102–125 mg/dL - Cardiovascular disease in a first- - Hyperuricemia degree relative (♂ <55 years; ♀ <65 - Obesity (BMI ≥ 30 kg/m² and/or, abdominal years) obesity (waist circumference ♂ ≥ 102 cm; ♀ ≥ 88 cm) - Family history of early onset of - Premature menopause arterial hypertension - Sedentary lifestyle - Psychosocial and socioeconomic factors - Heart rate >80/min at rest Clinical symptoms • Headache in the occiput • dizziness • floaters in the eyes or other visual disturbances • Nausea Asymptomatic end-organ damage - Pulse pressure (in an elderly individual) ≥ 60 mm Hg - Carotid-femoral pulse wave velocity >10 m/s - Left-ventricular hypertrophy: electrocardiographic signs (Sokolow–Lyon index >3.5 mV, etc.) and/or echocardiographic signs (left-ventricular mass index: ♂ >115 g/m²; ♀ ≥95 g/m²) - Advanced retinopathy (hemorrhges or exudates, papilledema) - Ankle–arm index <0.9 - Renal failure, moderate (eGFR >30–59 mL/min/1.73 m2) - Microalbuminuria (30–300 mg/24 hr or 30–300 mg/g creatinine) - Diabetes mellitus (Fasting blood glucose ≥ 126 mg/dL in at least two measurements and/or HbA1c >7% and/or Postprandial blood glucose ≥199 mg/dL) Established cardiovascular and kidney disease - Cerebrovascular disease: ischemic stroke, cerebral hemorrhage, TIA - Coronary artery disease: myocardial infarction, angina, myocardial revascularization - Presence of hemodynamically significant atheromatous plaque (stenosis) on imaging - Heart failure, including heart failure with preserved ejection fraction - Peripheral artery disease - Atrial fibrillation - Severe albuminuria > 300 mg/24 h or ACR (preferably in morning urine) >300 mg/g - CKD stage 4 and 5, eGFR < 30 mL/min/1.73m2
