Effect of selective blockade of catecholaminergic alpha and beta receptorson histamine-induced release of corticotropin and prolactin

We investigated the role of adrenergic receptors in histamine (HA)-induced release of corticotropin (ACTH) and prolactin (PRL) in conscious male rats. Specific alpha- or beta-receptor antagonists were administered intracerebr oventricularly in doses of 1 mmol at time -20 min, and HA (270 nmol), the H -1 receptor agonist 2-thiazolylethylamine (2-TEA; 2,180 nmol) or the H-2 re ceptor agonist 4-methylHA (4-MeHA; 790 nmol) were administered intracerebro ventricularly at -15 min. The animals were decapitated at 0 min, and plasma was analyzed for ACTH and PRL. Administration of HA and the histaminergic agonists stimulated ACTH secretion equally, while only HA and the H-2 recep tor agonist stimulated PRL secretion. Pretreatment with the adrenergic rece ptor antagonists had no effect on the ACTH response to the histaminergic co mpounds. In contrast, the PRL response to HA or 4-MeHA was inhibited or pre vented by the alpha-receptor antagonists phenoxybenzamine and phentolamine, the alpha(1)-receptor antagonist prazocin, the beta-receptor antagonist pr opranolol and the beta(1)-receptor antagonist atenolol, whereas the alpha(2 )-receptor antagonist yohimbine or the beta(2)-receptor antagonist ICI-118- 551 had no effect. The study indicates that histaminergic neurons interact with the catecholaminergic neuronal system in regulation of PRL secretion, and that this interaction is dependent upon activation of alpha(1)- and bet a(1)-receptors. In contrast, histaminergic neurons stimulate ACTH secretion independently of adrenergic receptor activation.