Involvement of histamine in the mediation of the stress-induced release of alpha-melanocyte-stimulating hormone in male rats.

The involvement of histaminergic neurons in the neuroendocrine regulation of the release of the pro-opiomelanocortin-derived peptides adrenocorticotropin (ACTH; anterior pituitary lobe) and alpha-melanocyte-stimulating hormone (alpha-MSH; intermediate pituitary lobe) was studied in conscious male rats. Pretreatment with the histamine (HA) synthesis inhibitor (S)-alpha-fluoromethylhistidine (100 mumol/kg i.p. at -6 h or 400 mumol/kg i.p. at -20 and -6 h) had no effect on basal ACTH release but decreased basal alpha-MSH release. The two doses of (S)-alpha-fluoromethylhistidine inhibited by 35 and 50% the ACTH response to inhibited the ACTH and alpha-MSH response to ether stress by 50 and 70%, respectively. Intracerebroventricular administration of the HA metabolism inhibitor SKF91488 (400 or 800 nmol at -15 min) stimulated basal secretion of ACTH and alpha-MSH dose-dependently and augmented slightly the restraint- and ether-stress-induced release of ACTH and alpha-MSH. Intracerebroventricular infusion of the H1 receptor antagonist mepyramine (0.37 mumol) or the H2 receptor antagonists cimetidine (0.40 mumol) or ranitidine (0.40 mumol) inhibited or prevented the alpha-MSH response to intracerebroventricular administration of HA (0.27 mumol), restraint or ether stress. Pretreatment with the dopamine receptor agonist bromocriptine or the beta-adrenergic receptor antagonist propranolol inhibited the alpha-MSH response to HA or stress. The results indicate that hypothalamic histaminergic neurons participate in the neuroendocrine regulation of the pro-opiomelanocortin-derived peptides from the anterior (ACTH) and intermediate (alpha-MSH) pituitary lobe of male rats.(ABSTRACT TRUNCATED AT 250 WORDS)