Histaminergic and catecholaminergic interactions in the central regulationof vasopressin and oxytocin secretion

Activation of histaminergic and noradrenergic/adrenergic neurons in the bra in stimulates the release of the neurohypophysial hormones arginine vasopre ssin (AVP) and oxytocin (OT) and are involved the mediation of the hormone responses to physiological stimuli such as dehydration and suckling. We the refore investigated whether the two neuronal systems interact in their regu lation of AVP and OT secretion in conscious male rats. When administered in tracerebroventricularly (icv), histamine (HA) as well as the H1 receptor ag onist 2-thiazolylethylamine or the H2 receptor agonist 4-methylHA stimulate d AVP and OT secretion. Prior icy infusion of antagonists specific to alpha or beta adrenergic receptors or their subtypes did not significantly affec t the hormone response to HA or the histaminergic agonists. Infused icy nor epinephrine (NE) or epinephrine (E) increased AVP and OT secretion. Prior i cy infusion of the H1 receptor antagonist mepyramine or the H2 receptor ant agonist cimetidine significantly inhibited the AVP and OT responses to NE a nd the AVP response to E, whereas only cimetidine inhibited the OT response to E significantly. Systemic pretreatment with imetit, which by activation of presynaptic H3 receptors inhibits neuronal synthesis and release of HA, decreased the AVP and OT responses to NE and E significantly. In the doses used, KA and E had no significant effect on mean arterial blood pressure. NE increased mean arterial blood pressure 10% at 1 and 2.5 min, whereafter the blood pressure returned to basal level within 10 min. The results indic ate that noradrenergic and adrenergic neurons stimulate AVP and OT secretio n via an involvement of histaminergic neurons, which may occur at magnocell ular neurons in the supraoptic and paraventricular nuclei of the hypothalam us. The stimulatory effect of the amines on neurohypophysial hormone secret ion seems to be independent of a central action on blood pressure. In contr ast, a functionally intact noradrenergic and adrenergic neuronal system see ms not to be a prerequisite for a HA-induced release of AVP and OT. The pre sent findings further substantiate the role of histaminergic neurons in the central regulation of neurohypophysial hormone secretion.