Effect of Selective Blockade of Catecholaminergic Alpha and Beta Receptors on Histamine-Induced Release of Corticotropin and Prolactin

Abstract

We investigated the role of adrenergic receptors in histamine (HA)-induced release of corticotropin (ACTH) and prolactin (PRL) in conscious male rats. Specific α- or β-receptor antagonists were administered intracerebroventricularly in doses of 1 mmol at time –20 min, and HA (270 nmol), the H₁ receptor agonist 2-thiazolylethylamine (2-TEA; 2,180 nmol) or the H₂ receptor agonist 4-methylHA (4-MeHA; 790 nmol) were administered intracerebroventricularly 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 H₂ receptor agonist stimulated PRL secretion. Pretreatment with the adrenergic receptor antagonists had no effect on the ACTH response to the histaminergic compounds. In contrast, the PRL response to HA or 4-MeHA was inhibited or prevented by the α-receptor antagonists phenoxybenzamine and phentolamine, the α₁-receptor antagonist prazocin, the β-receptor antagonist propranolol and the β₁-receptor antagonist atenolol, whereas the α₂-receptor antagonist yohimbine or the β₂-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 α₁- and β₁-receptors. In contrast, histaminergic neurons stimulate ACTH secretion independently of adrenergic receptor activation.

Effect of blockade of postsynaptic H1 or H2 receptors or activation of presynaptic H3 receptors on catecholamine-induced stimulation of ACTH and prolactin secretion

“…We have recently reported that blockade of a1 or b1 adrenoreceptors inhibited the PRL response to central administration of HA whereas the ACTH response to HA remained unaffected during central pretreatment with selective or non-selective a or b adrenoreceptor antagonists (17). Compared with the present study, we suggest that catecholamines and histamine interact in the central regulation of PRL secretion whereas the transmitters do not exert synergistic actions in the central regulation of ACTH secretion.…”

“…We have recently found that specific blockade of a1 and b1 adrenergic receptors inhibited the HA-induced PRL response (17), suggesting that HA interacts with catecholamines via these receptor subtypes in the regulation of PRL secretion. In contrast, we found that the ACTH response to HA was not affected by blockade of adrenergic receptors.…”