Role of Renal Prostaglandins and Relationship to Renin, Aldosterone, and Antidiuretic Hormone during Salt Depletion in Man*

Publisher Website
Google Scholar
Abstract
To study the relationship between urinary prostaglandins E2 (PGE2) and F2α, (PGF2α), aldosterone (UA) and arginine vasopressin and PRA and plasma aldosterone (PA), subjects were submitted to salt depletion under various conditions. When PGs were chronically suppressed by indomethacin treatment, spironolactone produced the expected natriuretic effect but failed to raise PRA, UA, and PA. When indomethacin was administered after several days of salt depletion, it induced a 50% decrement of PRA and lowered UA only slightly and nonsignificantly. The lack of effect of indomethacin on aldosterone was partially attributed to a concomitant rise of plasmab potassium. When indomethacin administration was started simultaneously with the salt restriction, all subjects achieved comparable sodium balance, but divergent hormonal responses were observed; PRA and UA rose in half of the subjects and did not change in the other half. Indomethacin administration and, consequently, suppression of urinary PGE2 and PGF2α were accompanied by a diminution of arginine vasopressin excretion in all situations. The data suggest that the temporal relationship between inhibition of PGs and stimulation of the renin-angiotensin-aldosterone system is an important determinant of the final effect on the latter system. Under conditions of suppression of endogenous PG synthesis, the organism can adapt normally to salt restriction without any elevation of renin or aldosterone. The observed lowering of urinary antidiuretic hormone levels is interpreted as an adaptation to the inhibition of PG biosynthesis known to potentiate the hydroosmotic effect of antidiuretic hormone.