[Prostaglandins may modulate the aldosterone response to ACTH in sodium restricted normotensives].

Aldosterone production following ACTH administration has been shown to be enhanced in sodium depletion. The mechanism(s) for this, however, is not entirely clear. Meanwhile, prostaglandins of the E series have been shown to stimulate steroidogenesis and urinary excretion of prostaglandin E2 and F2a in man, and PGI2 in the aortic wall of rats has been shown to increase in sodium depletion. In view of the above findings the present study was undertaken to evaluate the involvement of the endogenous prostaglandins in the augmentation of ACTH-induced aldosterone response during acute sodium depletion. Captopril was administered to elucidate the influence of the renin-angiotensin system (250mg q.i.d.) and Indomethacin (Ind) to suppress the production of the endogenous prostaglandins (200mg q.i.d.). Group I were on a diet containing 200mEq/day sodium and sodium depletion was achieved by a low sodium diet containing 60mEq/day sodium and oral treatment of fulosemide 80mg for 1 day (groups II, III and IV). Ind was given in group II, Ind + captopril in group III and captopril in group IV. The i.m. administration of 250/1g ACTH was performed at 0800-0900h. Body weight, serum sodium and potassium levels on the day of the experiment were significantly lower in groups II, III and IV versus group I. Basal PRA. in groups III and IV were more significantly elevated than groups I and II. Basal plasma 6-keto-PGF1a levels were significantly lower than in the Ind pretreated groups (II, III). There were no significant differences between baseline plasma aldosterone and cortisol concentrations. In groups I, II and III, plasma aldosterone increased from baseline levels to 182%, 134%, 193% respectively, following the ACTH administration, and there were no significant differences in mean increment among the three groups. In group IV, however, plasma