Atrial natriuretic peptide inhibits the stimulation of aldosterone secretion but not the transient increase in intracellular free calcium concentration induced by angiotensin II addition.
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 beta-[Asp1]angiotensin II (beta-[Asp1]AII), an AII analog, but markedly reduced the stimulated rate of aldosterone secretion. Consistent with these findings, radiolabeled 45Ca efflux stimulated by AII 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.
Apfeldorf
W J
WJ
Department of Cell Biology, Yale University School of Medicine, New Haven, Connecticut 06510.
Isales
C M
CM
Barrett
P Q
PQ
D000331:Aequorin / Q000378:metabolism; D000450:Aldosterone / Q000378:metabolism*; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D002217:Carbachol / Q000494:pharmacology; D002417:Cattle
D000804:Angiotensin II; D000450:Aldosterone; D000331:Aequorin; D009320:Atrial Natriuretic Factor; D002217:Carbachol; D002118:Calcium