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Dopaminergic Modulation of Aldosterone Secretion in the Rat

Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health Bethesda, Maryland 20205

Address requests for reprints to: Dr. Greti Aguilera, Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, Building 10, Room 8C407, National Institutes of Health, Bethesda, Maryland 20205.

Abstract

The dopamine antagonist metoclopramide (MCP) has been shown to acutely stimulate aldosterone secretion in vivo. To determine whether a dopaminergic mechanism is involved in the regulation of aldosterone secretion, we examined the effect of minipump infusion of MCP (iv) and/or angiotensin II (All; sc) upon plasma aldosterone, adrenal capsular All receptors, and 18-hydroxylase activity in rats maintained on high sodium intake. During normal sodium intake, plasma aldosterone was elevated from 8.3 ± 1.3 to 35.4 ± 3.2 µg/dl after 2-day infusion of a nonnatriuretic dose of All (25 µg/min) and to 15.0 ± 1.8 ng/dl after the infusion of 1.2 Mg/min MCP. All receptors were unchanged by MCP infusion, and rose from 1014 ± 98 to 1638 ± 98 fmol/mg after All infusion. During high sodium intake, the infusion of either All or MCP alone produced no change in plasma aldosterone or All receptors. However, after simultaneous infusion of All and MCP, plasma aldosterone rose from 4.5 ± 1.2 to 32.5 ± 2.7 ng/dl, All receptors increased from 969 ± 35 to 1607 ± 280 fmol/mg, and 18-hydroxylase activity, measured as the conversion of corticosterone to aldosterone by isolated mitochondria, rose from 29.5 ± 1.67 to 40.6 ± 2.9 pmol/mg·min. These adrenal responses induced by the combined treatment with All and MCP were similar to the effects of All infusion during normal sodium intake, indicating that MCP exerts a permissive action upon the trophic effects of All on the adrenal cell during high sodium intake. These actions of MCP were completely abolished by the simultaneous infusion of dopamine (2 µg/min), suggesting that the effects of MCP on adrenal function are due to its dopaminergic antagonist properties. In collagenase-dispersed adrenal glomerulosa cells, only supraphysiological concentrations of dopamine in the incubation medium (10–100 µM) inhibited basal, All-stimulated, and ACTH-stimulated aldosterone production, and these inhibitory effects were not reversed by high concentrations of MCP. Also, MCP itself inhibited both basal and stimulated aldosterone production. These results suggest that the stimulatory actions of MCP in vivo are exerted through liberation of other local regulators, rather than directly upon the adrenal glomerulosa cell. These findings have defined a mechanism by which the primary regulatory action of All upon aldosterone secretion can be modulated during high sodium intake by dopaminergic inhibition of adrenal glomerulosa function. (Endocrinology 114: 176, 1984)

Received March 17, 1983.

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