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Acute Effect of Captopril on Aldosterone Secretory Responses to Endogenous or Exogenous Adrenocorticotropin^*

Division of Nephrology and Endocrinology, Department of Internal Medicine, James A. Haley Veterans Administration Hospital, and the University of South Florida, College of Medicine Tampa, Florida 33612

Address requests for reprints to: German Ramirez, M.D. (111F), James A. Haley Veterans Administration Hospital, 13000 Bruce B. Downs Boulevard, Tampa, Florida 33612.

The aldosterone secretory response to Captopril (12.5 mg, orally) was studied in five normal men. Endogenous ACTH and epinephrine secretion was stimulated by the induction of hypoglycemia. Normally this stimulus increases plasma cortisol, GH, aldosterone, and PRA. Administration of captopril resulted in a blunted plasma aldosterone response to hypoglycemia, but no concomitant blunting of the plasma cortisol response. The responses of other hormones, with the exception of PRA, were not affected. When exogenous ACTH was administered to the same men with and without captopril, the plasma aldosterone response was again blunted by captopril, while the plasma cortisol response was unaffected. We conclude that angiotensin II may be required for ACTH to stimulate aldosterone secretion. Alternatively, the possibility that captopril may selectively inhibit aldosterone secretion at the adrenal cellular level cannot be excluded.

^* This work was supported in part by a grant from Squibb Corp. and the Renal Research and Education Fund of the University of South Florida, Tampa, FL.

Received May 28, 1987.

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