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Pathogenesis of arterial hypertension
Last reviewed: 06.07.2025
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Human blood pressure depends on a complex of various factors that constitute, according to the definition of academician P.K. Anokhin, a functional system. This system maintains blood pressure constancy according to the principle of self-regulation. In hypertension, an increase in blood pressure is caused by a complex interaction of genetic, psychosocial factors, as well as maladaptation of physiological mechanisms.
Disorders of the mechanisms of autoregulation of central hemodynamics
Normally, there are autoregulation mechanisms that maintain a balance between cardiac output and peripheral vascular resistance. Thus, with an increase in cardiac output during physical activity, total peripheral vascular resistance decreases. Conversely, with an increase in total peripheral vascular resistance, a reflex decrease in cardiac output occurs.
In hypertension, the mechanisms of autoregulation are impaired. There is a discrepancy between cardiac output and total peripheral vascular resistance. In the early stages of hypertension, an increase in cardiac output is detected, while total peripheral vascular resistance may be normal or only slightly increased. As the disease progresses and systemic arterial pressure stabilizes at high levels, total peripheral vascular resistance steadily increases.
Systemic arterial pressure begins to increase with the exhaustion of antihypertensive homeostatic mechanisms or with excessive strengthening of vasoconstrictor and antinatriuretic neurohumoral systems (angiotensin II, norepinephrine, endothelin-I, insulin, etc.). Among the antihypertensive homeostatic mechanisms, the following are of great importance:
- renal excretion of sodium ions;
- baroreceptors of the aorta and large arteries;
- activity of the kallikrein-kinin system
- release of dopamine, natriuretic peptides A, B, C;
- prostaglandins E 2 and I 2,
- nitric oxide;
- adrenomedullin;
- taurine.
Disruption of the renin-angiotensin-aldosterone system
Renin is a serine protease synthesized in the juxtaglomerular apparatus of the kidneys, it is also formed in the cells of other organs, in particular the adrenal cortex. The secretion of renin is affected by a decrease in blood pressure, sodium deficiency in the body, kallikrein, endorphins, beta-adrenergic stimulation, vasodilators. Renin breaks down the protein molecule angiotensinogen, converting it into angiotensin I. This decapeptide is biologically inactive, but after exposure to ACE it becomes an active octapeptide, which is called angiotensin II. ACE is secreted by cells of the lungs and blood vessels.
Angiotensin II causes vasoconstriction and stimulates the secretion of aldosterone by the adrenal cortex, resulting in increased sodium reabsorption in renal tubule cells, followed by an increase in circulating plasma volume and an increase in blood pressure. A potent agent that inhibits aldosterone secretion is atrial natriuretic factor.
Increased activity of the renin-angiotensin-aldosterone system in the bloodstream and tissues plays an important role in the pathogenesis of hypertension. Epidemiological studies have shown that plasma renin levels serve as an independent prognostic factor for the course of arterial hypertension. With a high renin level, the risk of complications of hypertension is 6 times higher.