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- W2286720476 abstract "Parenteral administration of progesterone in normal man provokes an increased sodium and chloride urinary secretion during the 1st days of treatment with no change in kaliuresis. This effect is antagonist to aldosterone. Like spironolactone, progesterone competes with the mineralcorticoid cytoplasmic receptor of renal distal tubular cells. The lack of net variation of kaliuresis under progesterone remains however ill understood. In the healthy subject progesterone-induced natriuresis stimulates plasma renin activity and secondary aldosteronism restricts the amplitude of total sodium loss. Progesterone action may therefore account for the stimulation of the angiotensin renin system during the luteal phase of the menstrual cycle and also contribute to the increased aldosterone secretion during pregnancy. Its pathogenetic role in premenstrual edema is controversial. 17-hydroxyprogesterone which is secreted in large amounts during adrenal hyperplasia due to a block of 21 hydroxylase, has a natriuretic action comparable to that of progesterone, which accounts for the constant activation of the renin system in that condition. Synthetic progestatives do not have the natriuretic action of progesterone; their affinity for the renal tubular receptor in vitro is very small or nil. They do not, however, seem to account for the arterial hypertension observable with the estroprogestative pill. They should be used with care in the woman with hypertension. On the other hand, oral contraception with continuous minimal doses of progestatives seem quite well tolerated with regard to blood pressure. (author's modified)" @default.
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- W2286720476 date "1981-04-01" @default.
- W2286720476 modified "2023-09-23" @default.
- W2286720476 title "[Progesterone, progestatins and water and sodium metabolism]." @default.
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