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Atrial Natriuretic Peptide Inhibits the Stimulation of Aldosterone Secretion But Not the Transient Increase in Intracellular Free Calcium Concentration Induced by Angiotensin II Addition^*

Departments of Cell Biology and Internal Medicine, Yale University School of Medicine New Haven, Connecticut 06510

Address request for reprints to: Dr. Paula Q. Barrett, Department of Internal Medicine, Yale University School of Medicine, P.O. Box 3333, New Haven, Connecticut 06510.

Abstract

The effect of atrial natriuretic peptide (ANP) on cellular calcium metabolism was evaluated in bovine adrenal glomerulosa cells stimulated by agonists that use the Ca²⁺- phosphoinositide messenger system. The calcium-sensitive probe aequorin was used to measure intracellular free calcium concentration, and the aldosterone secretory rate was simultaneously monitored. ANP did not block the calcium transient induced by β-[Asp¹]angiotensin II (β-[Asp¹]All), an All analog, but markedly reduced the stimulated rate of aldosterone secretion. Consistent with these findings, radiolabeled ⁴⁵Ca efflux stimulated by All and carbachol was not altered by the concurrent addition of ANP. These results indicate that ANP has no effect on the phosphoinositide-mediated calcium transient and the associated rise in cellular calcium efflux, suggesting that these parameters of calcium metabolism are not the locus of ANP's inhibitory action. (Endocrinology 122: 1460–1465,1988)

Footnotes

^* This work was supported in part by grants from the Medical Scientist Training Program of the National Institutes of General Science (GM-07205), the American Heart Association (AHA-861014), and the NIH (AM-33001). This work will be submitted in partial fulfillment of the requirements for a Ph.D. degree at Yale University.

Received February 17, 1987.

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