Effects of β-Lipotropin and β-Lipotropin-derived Peptides on Aldosterone Production in the Rat Adrenal Gland

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Abstract

To investigate the role of non-ACTH pituitary peptides on steroidogenesis, we studied the effects of synthetic β-lipotropin, β-melanotropin, and β-endorphin on aldosterone and corticosterone stimulation using rat adrenal collagenase-dispersed capsular and decapsular cells. β-lipotropin induced a significant aldosterone stimulation in a dose-dependent fashion (10 nM-1 μM). β-endorphin, which is the carboxyterminal fragment of β-lipotropin, did not stimulate aldosterone production at the doses used (3 nM-6 μM). β-melanotropin, which is the middle fragment of β-lipotropin, showed comparable effects on aldosterone stimulation. β-lipotropin and β-melanotropin did not affect corticosterone production in decapsular cells. Although ACTH1-24 caused a significant increase in cyclic AMP production in capsular cells in a dose-dependent fashion (1 nM-1 μM), β-lipotropin and β-melanotropin did not induce an increase in cyclic AMP production at the doses used (1 nM-1 μM). The β-melanotropin analogue (glycine[Gly]10-β-melanotropin) inhibited aldosterone production induced by β-lipotropin or β-melanotropin, but did not inhibit aldosterone production induced by ACTH1-24 or angiotensin II. Corticotropin-inhibiting peptide (ACTH7-38) inhibited not only ACTH1-24 action but also β-lipotropin or β-melanotropin action; however it did not affect angiotensin II-induced aldosterone production. (saralasin [Sar]1; alanine [Ala]8)-Angiotensin II inhibited the actions of β-lipotropin and β-melanotropin as well as angiotensin II. These results indicate that (a) β-lipotropin and β-melanotropin cause a significant stimulation of aldosterone production in capsular cells, (b) β-lipotropin and β-melanotropin have a preferential effect on zona glomerulosa cells, (c) β-melanotropin contains the active peptide core necessary for aldosterone stimulation, (d) the effects of these peptides on aldosterone production may be independent of cyclic AMP, and (e) the receptors for β-lipotropin or β-melanotropin may be different from those for ACTH or angiotensin II.

Authors

Hiroaki Matsuoka, Patrick J. Mulrow, Roberto Franco-Saenz