Adrenergic regulation of alpha-MSH secretion in man: evidence for a stimulatory role of beta-receptors
Limone, P.; D'Alessandro, V.; Rainero, I.; Ambrogio, C.; Pinessi, L.; De Gennaro, T.; Molinatti, G.M.
Acta Endocrinologica 128(2): 150-155
1993
ISSN/ISBN: 0001-5598 PMID: 8383904 Document Number: 411993
In several animals species the catecholamines stimulate the release of alpha-MSH from medlanotrope cells of the pituitary neurointermediate lobe through beta-receptors. The human hypophysis does not include a well-defined intermediate lobe and the methods for measuring alpha-MSH are often poorly sensitive. Neuroregulation of this hormone in man has thus received little attention. To see whether the adrenergic system is involved in the control of alpha-MSH secretion and whether the latter is independent of that of other peptides derived from proopiomelanocortin, such as ACTH, we studied the effects on plasma alpha-MSH-like immunoreactivity (alpha-MSH-LI), ACTH, and cortisol of some adrenergic drugs active on the beta-receptors. Six normal volunteers underwent the infusion of the following drugs: isoproterenol (0.03 mu-g cntdot kg-1 cntdot min-1 for 60 min), proprandiol (1 mg cntdot min-1 for 5 min followed by 0.1 mg cntdot min-1 for 115 min), propranolol + isoproterenol (infused between 30 and 90 min of propranolol infusion), placebo (saline solution). Isoproterenol increased alpha-MSH-LI at 15 min (p lt 0.001). Propranolol induced a fall of alpha-MSH-LI between 30 and 60 min (p lt 0.001), followed by a return to preinfusion concentrations beginning at 75 min, and completely prevented the stimulatory effect of isoproterenol. Plasma ACTH and serum cortisol were always unaffected. These results indicate that in man the adrenergic system stimulates alpha-MSH-LI release through beta-receptors, and that alpha-MSH-LI secretion is dissociated from that of ATH and cortisol. This in turn suggests that separate neuroregulatory mechanisms exist for the melanotrope and carticotrope cells.