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SUMMARY
Prostaglandin E2 increased aldosterone output by superfused capsular adrenal glands obtained from sodium-repleted, hypophysectomized rats but corticosterone did not show a statistically significant increase. Prostaglandin A2 increased corticosterone but not aldosterone production by incubated capsular glands obtained from sodium-repleted, hypophysectomized rats. Both aldosterone and corticosterone production rates were increased by PGA2 after previous sodium restriction. Corticosterone production rate of the decapsulated adrenal gland was not significantly modified by prostaglandin A2 in a concentration effective on the capsular adrenal gland. A possible role of prostaglandins in the regulation of aldosterone secretion is discussed.
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Department of Physiology, Semmelweis University Medical School, 1444 Budapest 8, POB 259, Hungary
(Received 30 November 1976)
Prostaglandins (PG) of the A-type selectively stimulate the aldosterone secretion rate in man (Fichman, Littenburg, Brooker & Horton, 1972) and aldosterone production rate in the rat (Spät & Józan, 1975). Since PGA escapes inactivation by pulmonary tissue (McGiff, Terragno, Strand, Lee, Lonigro & Ng, 1969), this compound or an active metabolite of it may function as a hormone in the circulation. In view of its zonal specificity and its action in the early stage of aldosterone biosynthesis (Spät & Józan, 1975) as well as the increased plasma level of immunoreactive PGA during sodium depletion (Lee, 1973; Zusman, Forman, Schneider, Caldwell, Speroff & Mulrow, 1973), a mediating function may be postulated for PGA in acute fluid depletion-induced hyperaldosteronism. To test this possibility we examined the effect of diuretic treatment on peripheral aldosterone concentration with
