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

The effect of inhibition of the neuronal histaminergic system by blockade o f postsynaptic H1 or H2 receptors or activation of presynaptic H3 autorecep tors on the ACTH and prolactin responses to the catecholamines epinephrine and norepinephrine was investigated in conscious male rats. Intracerebroven tricular infusion of epinephrine and norepinephrine stimulated ACTH and pro lactin secretion. Prior intracerebroventricular infusion of the H1 receptor antagonist, mepyramine, or the H2 receptor antagonist, cimetidine, had no effect on the ACTH response to epinephrine or norepinephrine, while these r esponses were inhibited by pretreatment with the H3 receptor agonist, imeti t. The prolactin response to norepinephrine was significantly inhibited by pretreatment with mepyramine, cimetidine or imetit whereas the three histam inergic compounds had no effect on the prolactin response to epinephrine. T he findings suggest that the histaminergic system exerts a mediating or per missive action on the norepinephrine-induced stimulation of prolactin secre tion, whereas an intact histaminergic system may not be required for catech olamines to stimulate ACTH secretion. The inhibitory effect of imetit on ca techolamine-induced release of ACTH may be due to an activation of H3 recep tors located presynaptically on non-histaminergic neurons, e.g, aminergic n eurons. The study further indicates an important role of histamine in the n euroendocrine regulation of prolactin secretion.