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Dispersed chick adrenocortical cells were incubated with mammalian and avian angiotensin-II, Ca²⁺, K⁺, verapamil, nifedipine, Ca²⁺ ionophore (A23187 [GenBank] ), protein kinase-C activator (phorbol 12-myristate 13-acetate; TPA), atrial natriuretic peptide (ANP), sodium nitroprusside (SNP) and ACTH. Secretion of aldosterone and corticosterone, and accumulation of cyclic nucleotides were assessed.

Secretion of aldosterone was not affected by angiotensin-II, Ca²⁺ channel blockers, Ca²⁺ ionophore or TPA. ANP stimulated production of cyclic GMP (cGMP), and inhibited aldosterone secretion with a similar dose–response relationship. SNP also stimulated cGMP production and inhibited the ACTH-stimulated aldosterone secretion. The results indicate that ANP is an inhibitor of aldosterone secretion in birds and suggest that this inhibition is mediated by cGMP. In contrast to mammalian glomerulosa cells, angiotensin-II and the calcium-inositol phosphate-protein kinase C pathway appear not to be involved in the regulation of aldosterone secretion by avian adrenal cells.

J. Endocr. (1988) 118, 447–453