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Effect of Human βEndorphin on Plasma Aldosterone Concentrations in Normal Human Subjects^*

Departments of Medicine, University of Oklahoma Health Sciences Center Oklahoma City, Oklahoma 73126 Veterans Administration Hospital Medical Center
University of Texas Health Sciences Center, and Veterans Administration Hospital Medical Center at Dallas Dallas, Texas 75216
Laboratory of Molecular Endocrinology, University of California City, California 94143

Address requests for reprints to: Dr. Allan Glass, Kyle Metabolic Unit, Walter Reed Army Medical Center, Washington, D. C. 20012.

β-Endorphin recently was proposed as a possible physiological stimulus of aldosterone secretion based on studies in animals. Since human β-endorphin (β_h-endorphin) does not contain the ACTH-(4-10) homology common to other ACTH-related neuropeptides that stimulate aldosterone, its mechanism of stimulation might differ from that of the other peptides. In the present study, we infused β_h-endorphin into six normal subjects under carefully controlled conditions at dosage levels several orders of magnitude higher than endogenous levels. No increase in plasma aldosterone was found in these subjects ingesting a normal sodium intake despite the fact that other biological actions of β_h-endorphin were manifest. By contrast, an equimolar infusion of ACTH-(1–24) caused a significant increase in plasma aldosterone. These studies do not support a significant role for β_h-endorphin in control of aldosterone secretion in man and are consistent with the concept that the ACTH-(4–10) amino acid sequence, common to ACTH, β-lipotropin, -lipotropin, βMSH, and MSH, is a major determinant of their aldosterone-stimulating capacity.

^* The opinions and assertions herein are the private views of the authors and are not to be construed as official or representing the views of the Departmentof the Army or the Department of Defense. This work was supported by the Clinical Investigation Service, Walter Reed Army Medical Center.

Received July 17, 1984.