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Research Article Free access | 10.1172/JCI110311
Department of Medicine, Medical College of Ohio, Toledo, Ohio 43699
Hormone Research Laboratory, University of California, San Francisco, California 94143
Find articles by Matsuoka, H. in: JCI | PubMed | Google Scholar
Department of Medicine, Medical College of Ohio, Toledo, Ohio 43699
Hormone Research Laboratory, University of California, San Francisco, California 94143
Find articles by Mulrow, P. in: JCI | PubMed | Google Scholar
Department of Medicine, Medical College of Ohio, Toledo, Ohio 43699
Hormone Research Laboratory, University of California, San Francisco, California 94143
Find articles by Franco-Saenz, R. in: JCI | PubMed | Google Scholar
Published September 1, 1981 - More info
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.