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

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Abstract
β-Endorphin recently was proposed as a possible physiological stimulus of aldosterone secretion based on studies in animals. Since human β-endorphin (βh-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 βh-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 βh-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 βh-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, γ-lipotropin, βMSH, and αMSH, is a major determinant of their aldosterone-stimulating capacity.