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Journal of Clinical Endocrinology & Metabolism, Vol 51, 64-69, Copyright © 1980 by Endocrine Society
ARTICLES |
RH Noth, RW McCallum, C Contino and J Havelick
To investigate the interaction between dopamine and aldosterone in man, either the dopamine antagonist, metoclopramide [methoxy-2-chloro-5- procainamide (M)], or a placebo was given by an iv bolus in a random, double blind fashion to nine supine volunteers on a hospital diet (mean urinary sodium excretion, 135 +/- 17 vs. 145 +/- 26 meq/24 h; P = NS). After M (10 mg), plasma aldosterone (PA) rose from 6.4 +/- 1.1 to 14.0 +/- 2.2 (SEM) ng/dl (P less than 0.01) within 15 min. PRA, potassium, and cortisol were unchanged. PRL increased 10-fold, but individual increments in PA and PRL did not correlate significantly. Oral M (10 mg) produced a rise in PA in only two of five volunteers. To determine whether the increase in PA was due to the dopamine antagonist properties of M, the iv study was repeated in four of the volunteers during an ongoing dopamine infusion. The integrated incremental change in PA during the hour after M administration was markedly blunted (399 +/- 56 vs. 69 +/- 32 ng/dl.min; P less than 0.05), and the PRL response was totally abolished. Assuming no major effects of M on the MCR of aldosterone, these data suggest a tonic inhibitory influence of dopamine on aldosterone secretion.
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