TY - JOUR

T1 - Effect of selective blockade of catecholaminergic alpha and beta receptors on histamine-induced release of corticotropin and prolactin

AU - Willems, Edwin

AU - Knigge, Ulrich

AU - Jørgensen, Henrik

AU - Kjær, Andreas

AU - Warberg, Jørgen

PY - 1999

Y1 - 1999

N2 - 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; 2180 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.

AB - 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; 2180 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.

KW - Catecholamine receptors

KW - Corticotropin

KW - Histamine

KW - Histamine receptors

KW - Prolactin

UR - http://www.scopus.com/inward/record.url?scp=0032967920&partnerID=8YFLogxK

U2 - 10.1159/000054432

DO - 10.1159/000054432

M3 - Journal article

C2 - 10343171

AN - SCOPUS:0032967920

VL - 69

SP - 309

EP - 315

JO - Neuroendocrinology

JF - Neuroendocrinology

SN - 0028-3835

IS - 5

ER -