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Dopamine Inhibits the Aldosterone Response to Upright Posture^*

CARL D. MALCHOFF, JOSEPH HUGHES, SUBHA SEN, SANDRA JACKSON and ROBERT M. CAREY

Department of Medicine, University of Virginia Medical Center Charbttesville, Virginia 22908 Research Division, The Cleveland Clinic Foundation Cleveland Ohio 44106.

Address requests for reprints to: Dr. Robert M. Carey, Box 482, University of Virginia Medical Center, Charlottesville, Virginia 22908.

Aldosterone secretion in man is stimulated by potassium, ACTH, and angiotensin II and is inhibited by dopamine (DA). In normal sodium-replete supine individuals, aldosterone secretion is under maximum tonic inhibition by DA. Dopaminergic control of aldosterone secretion is modified by dietary sodium depletion. To determine the physiological significance of dopaminergic inhibition of aldosterone secretion, we studied the effect of DA on the aldosterone response to upright posture.

Twelve normal men were studied while eating an ad libitum sodium diet, and the effect of DA was determined in the supine and upright positions. Plasma aldosterone (PAC), plasma cortisol (F), plasma aldosterone-stimulating factor (ASF), PRA, and blood pressure were measured while the men were supine and after 4 h of upright posture during an infusion of 5% dextrose vehicle and during a DA infusion of 4.0 µg/kg-min. The men also were studied as a time control in the supine position while receiving vehicle or DA. PAC increased from a mean basal value of 20.4 ± 3.2 ng/dl (±SE) by 25.9 ± 5.1 ng/dl to a peak of 44.4 ± 2.4 ng/dl in response to upright posture during vehicle infusion. The PAC response to upright posture was reduced to 7.4 ± 1.8 ng/dl (P < 0.05) when DA was infused. The increase in PRA with upright posture was 3.7 ± 1.3 ng/ml-h during the vehicle infusion and 4.1 ± 1.1 ng/ml-h (P = NS) during the DA infusion. ASF, F, and blood pressure were not altered by upright posture and DA. PAC did not change in the six men infused with DA while supine. Therefore, DA inhibits upright aldosterone responses without affecting PRA, ASF, or F.

^* This work was supported by USPHS General Clinical Research Center Grant RR-847 and NIH Grant R01-HL-32188. Data processing and analysis were made possible by NIH CLINFO Grant M01-RA- 00847.

Recipient of a postdoctoral fellowship from the Juvenile Diabetes Foundation.

Received August 20, 1985.

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