Atrial natriuretic peptide inhibits the stimulation of aldosterone secretion but not the transient increase in intracellular free calcium concentration induced by angiotensin ii addition

William J. Apfeldorf, Carlos M. Isales, Paula Q. Barrett

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1460-1465
Number of pages6
JournalEndocrinology
Volume122
Issue number4
DOIs
StatePublished - Apr 1 1988
Externally publishedYes

ASJC Scopus subject areas

  • Endocrinology

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