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Pathogenesis of arterial hypertension
Last reviewed: 19.10.2021
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Arterial pressure in a person depends on a complex of various factors, which, according to Academician P.K. Anokhin, a functional system. This system maintains the consistency of blood pressure by the principle of self-regulation. In hypertensive disease, the increase in blood pressure is caused by a complex interaction of genetic, psychosocial factors, as well as maladaptation of physiological mechanisms.
Disorders of autoregulation mechanisms of central hemodynamics
Normally, there are autoregulation mechanisms that support the balance between cardiac output and peripheral vascular resistance. Thus, with an increase in cardiac output during exercise, the overall peripheral vascular resistance decreases. On the contrary, with an increase in the total peripheral vascular resistance, a reflex decrease in cardiac output occurs.
With hypertension, the mechanisms of autoregulation are violated. There is a discrepancy between cardiac output and total peripheral vascular resistance. In the early stages of hypertension, cardiac output is increased, while the overall peripheral vascular resistance may be normal or only slightly elevated. As the disease progresses, the systemic arterial pressure stabilizes at high levels, the overall peripheral vascular resistance increases steadily.
Systemic arterial pressure begins to increase with the depletion of antihypertensive homeostatic mechanisms, or with excessive strengthening of vasoconstrictor and antinatriuretic neurohumoral systems (angiotensin II, norepinephrine, endothelium-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 kallikrein-kinin system
- release of dopamine, natriuretic peptides A, B, C;
- prostaglandins E 2 and I 2,
- Nitric oxide;
- adrenomedullin;
- taurine.
Violation of the activity 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 lower blood pressure, sodium deficiency in the body, kallikrein, endorphins, beta-adrenergic stimulation, vasodilators. Renin cleaves the protein molecule of angiotensinogen, converting it to angiotensin I. This decapeptide is not biologically active, but after exposure to ACE it becomes an active octapeptide, called angiotensin II. ACE is secreted by cells of the lungs and blood vessels.
Angiotensin II causes vasoconstriction (vasoconstriction), as well as stimulates the secretion of aldosterone by the adrenal cortex, resulting in increased sodium reabsorption in the cells of the renal tubules, followed by an increase in the volume of circulating plasma and increased blood pressure. A potent agent that inhibits the secretion of aldosterone is the atrial natriuretic factor.
The increased activity of the renin-angiotensin-aldosterone system in the blood stream and tissues plays an important role in the pathogenesis of hypertensive disease. In epidemiological studies, it has been shown that plasma renin level serves as an independent prognostic factor in the course of arterial hypertension. With a high level of renin in 6 times the risk of complications of hypertension.