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Differing Effects of Metoclopramide and Adrenocorticotropin on Plasma Aldosterone Levels in Glucocorticoid-Suppressible Hyperaldosteronism and Other Forms of Hyperaldosteronism^*

ARUNABHA GANGULY, J. HOWARD PRATT, MYRON H. WEINBERGER, CLARENCE E. GRIM and NAOMI S. FINEBERG

Departments of Medicine, University of South Florida College of Medicine, The James A. Haley Veterans Hospital Tampa, Florida 33612
Indiana University School of Medicine, and Veterans Administration Hospital Indianapolis, Indiana 46202

Address all correspondence and requests for reprints to: Arunabha Ganguly, M.D., University of South Florida College of Medicine, Veterans Administration Hospital (111-M), 13000 N. 30th Street, Tampa, Florida 33612.

To investigate possible dopaminergic effects on aldosterone production, we administered the dopamine antagonist metoclopramide to 11 normal subjects, 8 patients with primary aldosteronism due to adenoma or hyperplasia, and 5 other patients with the glucocorticoid-suppressible form of hyperaldosteronism (GSH). All subjects except for those with GSH responded to metoclopramide with an increase in plasma aldosterone concentration even when endogenous ACTH was suppressed by dexamethasone pretreatment. This increase occurred without apparent mediation of other recognized stimuli for aldosterone secretion. In contrast, the patients with GSH failed to show any aldosterone response while receiving dexamethasone, but demonstrated a rise in plasma aldosterone concentrationconcentration when dexamethasone was withheld. The responses in the patients with both forms of primary aldosteronism were greater in magnitude than in the normal subjects or in the subjects with GSH when not receiving dexamethasone. These studies, while demonstrating differences between the subtypes of hyperaldosteronism in their responsiveness to metoclopramide, indicate that ACTH or some other factor may exert a permissive effect in GSH for the aldosterone response to metoclopramide. A graded infusion of ACTH revealed a greater aldosterone response in GSH compared to that in the other groups, further suggesting the importance of ACTH in this disorder.

^* This work was supported by USPHS Grants HL-14159, (Specialized Center of Research in Hypertension), RR-00750 (General Clinical Research Center), and HL-27294.

Partially supported by the V.A. Hospital.

Received November 12, 1982.

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