Premenstrual hypertension is a secondary form of hypertension that occurs periodically during the menstrual period and is provoked by heavy bleeding. Premenstrual hypertension is more common in women 20-30 years of age.
Etiology pathogenesis
In pathophysiological studies, detection and study of the sources of hypertension is of great importance. In postmenopause, blood pressure is no longer due only to the excretion of sodium and an increase in circulating blood volume after menstruation. Basically we are talking about stress or sympathetic hyperreactivity of the adrenal glands and the lack of adequate contraceptive resistance. The latter should be explained by the extinction of ovarian depressor hormones.
The menopause period is accompanied by profound changes in hormonal status. Menstruation stops, anovulatory cycles occur, and the neuroendocrine activity of the ovaries is inhibited. The cessation of the negative effect of progesterone leads to a sharp increase in the activity of adrenal androgens. The level of aldosterone in the blood and the volume of circulating fluid decreases.
To explain the mechanism of premenstrual arterial hypertension, two points of view are considered dominant. * Orthostatic hypertension. An increase in blood pressure is associated with a decrease in the tone of large arteries - vasoconstrictors, which explains the occurrence of periodic orthostatic increases in blood pressure during the premenstrual cycle. Lack of estrogen contributes to the development of peripheral vasopression and makes the distal arteries especially vulnerable, which are especially vulnerable against the background of estrogen deficiency. Impaired serotonin metabolism and a decrease in aldosterone levels can lead to decreased vascular tone. The influence of changes in ovarian estrogenic function on the regulation of blood pressure levels, as well as the impact of the stress response when pain occurs, is assumed.
* Hormonal theory, based on data on biochemical changes in the ovarian-pituitary system in the premenstrual phase, changes in redox processes and hormone synthesis. In fact, these are various modifications of one hypothesis about an increased predisposition to the occurrence of premenstrual syndromes, causing not only depression, but also impaired peripheral circulation, in particular, the syndrome of Frustrated Hopes. Hence the adaptive changes in the system that react according to the feedback principle: increasing the threshold of perception, reducing the time of contact of target organs with endogenously formed decay products, increasing their final volume and concentration in tissues. According to this hypothesis, only with reduced sensitivity of receptors to estrogen is it possible to increase blood pressure at the beginning of the cycle.