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Pathogenesis of arterial hypotension
Last reviewed: 06.07.2025
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The most complex and poorly studied issues remain the pathogenesis of arterial hypotension. There are several theories of the origin of the disease: constitutional-endocrine, vegetative, neurogenic, humoral.
Constitutional-endocrine theory
According to this theory, arterial hypotension occurs due to a primary decrease in vascular tone due to insufficient function of the adrenal cortex. Subsequent studies have shown that arterial hypotension is accompanied by a decrease in mineralocorticoid, glucocorticoid, and androgenic functions of the adrenal glands. In younger schoolchildren with stable arterial hypotension, the glucocorticoid function of the adrenal cortex is decreased, and in older schoolchildren, the glucocorticoid and mineralocorticoid functions are decreased.
Vegetative theory
According to the vegetative theory, the occurrence of arterial hypotension is associated with an increase in the function of the cholinergic system and a decrease in the function of the adrenergic system. Thus, most patients with arterial hypotension have an increase in the content of acetylcholine and a decrease in the level of catecholamines in the blood plasma and daily urine. It is known that the lack of synthesis of norepinephrine and its precursors contributes to a decrease in diastolic and mean arterial pressure. Variability in the synthesis of these neurotransmitters is typical for the pre- and pubertal periods. Hypofunction of the sympathetic-adrenal system leads to variability in the parameters of blood supply to the brain and central circulation, impaired external respiration, and a decrease in oxygen consumption. In recent years, it has been established that in the origin of arterial hypotension, it is not so much a decrease in the tone of the sympathetic-adrenal system that matters, but a change in the sensitivity of alpha- and beta-adrenoreceptors to neurotransmitters.
Neurogenic theory
This theory of the origin of arterial hypotension is currently recognized by most researchers. Violation of the neurogenic pathway of arterial pressure regulation is the main link in the origin of arterial hypotension. According to this theory, under the influence of psychogenic factors, changes in neurodynamic processes in the cerebral cortex occur, a violation of the relationship between the processes of excitation and inhibition both in the cortex and in the subcortical vegetative centers of the brain (i.e., a unique form of neurosis occurs). Because of this, hemodynamic disorders occur, the most important of which is considered to be dysfunction of the capillaries with a decrease in total peripheral resistance. In connection with the resulting functional disorders, compensatory mechanisms come into play, which lead to an increase in the stroke and minute volume of blood. In more than 1/3 of adult patients with stable arterial hypotension, inhibition processes in the cerebral cortex prevail over excitation processes, dysfunction of the upper parts of the brainstem is typical, and the a-index on the background electroencephalogram decreases during functional tests.
In most cases of arterial hypotension, existing instrumental and biochemical methods fail to detect specific causes of the disease. However, there is no doubt that in hypotonic disease, a decrease in arterial pressure is associated with a complex interaction of genetic factors, as well as a violation of physiological regulatory mechanisms.
In arterial hypotension, autoregulation mechanisms are impaired. A discrepancy arises between cardiac output and total peripheral vascular resistance. In the early stages of the disease, cardiac output is increased, while total peripheral vascular resistance is decreased. As the disease progresses and systemic arterial pressure is established at a low level, total peripheral vascular resistance steadily decreases.
Humoral theory
In recent years, in connection with the study of the problem of regulation of arterial pressure, interest in the study of humoral factors of a depressor nature has increased. According to the humoral theory, arterial hypotension is caused by an increase in the level of kinins, prostaglandins A and E, which have a vasodepressor effect. A certain significance is attached to the content of serotonin and its metabolites in the blood plasma, participating in the regulation of arterial pressure.
Systemic arterial pressure begins to decrease with the activation of antihypertensive homeostatic mechanisms (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 E2 and I2 , nitric oxide, adrenomedulin, taurine).
Thus, primary arterial hypotension is currently considered as a special form of neurosis of the vasomotor center with dysfunction of the peripheral depressor apparatus and secondary changes in the function of the adrenal glands.
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