Dissociation of osmotic and ionic modulation of aldosterone secretion

Abstract

Although other investigators have suggested that reductions in either Na or chloride concentration stimulate aldosterone secretion, we previously found that small reductions in NaCl (3-7 mM) that enhanced angiotensin II-(ANG II) and [K]- but not adrenocorticotropic hormone (ACTH)-stimulated aldosterone secretion are due to a change in osmolality. In the present study, aldosterone secretion by an isolated perfused canine adrenal gland was stimulated by low doses of ANG II or ACTH or by small increases in perfusate [K], and during this stimulation, replacing 25 mM NaCl with an isosmotic amount of mannitol enhanced aldosterone secretion induced by each of the above secretagogues. Choline chloride significantly enhanced ANG II-stimulated aldosterone secretion when used in place of 25 mM NaCl, but sodium methylsulfate did not. Large isosmotic reductions in [NaCl] failed to alter ACTH-stimulated cortisol secretion or the conversion of either exogenous corticosterone or 11-deoxycorticosterone to aldosterone. Thus, reductions in Na, but not in chloride concentration, specifically enhance the ability of the adrenal glomerulosa to secrete aldosterone in response to ANG II, K, and ACTH by an action on some site in the steroidogenic cascade that is sensitive to ANG II, potassium, and ACTH.