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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