A Role for β-Melanotropin in the Regulation of Aldosterone Secretion during Sodium Deficiency in the Rat

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Abstract
1. The effect of sodium deficiency on adrenal sensitivity to β-melanotropin (β-melanocyte stimulating hormone; β-MSH) and the effect of β-MSH on a late step of aldosterone biosynthesis were studied using collagenase-dispersed rat adrenal cells. 2. Sodium depletion enhanced the sensitivity of the adrenal glomerulosa cells to β-MSH, resulting in a shift of the dose-response curve to the left, so that doses of β-MSH within the physiological range caused significant stimulation of aldosterone production. 3. The aldosterone level obtained by maximum doses of β-MSH was similar to that obtained after angiotensin (‘angiotensin II’; ANGII) during sodium depletion. 4. Sodium depletion did not change the corticosterone response to β-MSH by decapsular cells. 5. Similarly to ANGII, β-MSH significantly stimulated the conversion of exogenous corticosterone into aldosterone in the presence of an inhibitor of 3β-hydroxysteroid dehydrogenase, WIN 19,578. 6. These data suggest that β-MSH or peptides containing β-MSH may play a role in the regulation of aldosterone secretion during sodium depletion in the rat and that β-MSH increases aldosterone production partly by stimulating the late step in aldosterone biosynthesis, the conversion of corticosterone into aldosterone.

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