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 of postsynaptic H1 or H2 receptors or activation of presynaptic H3 autoreceptors on the ACTH and prolactin responses to the catecholamines epinephrine and norepinephrine was investigated in conscious male rats. Intracerebroventricular infusion of epinephrine and norepinephrine stimulated ACTH and prolactin 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 responses were inhibited by pretreatment with the H3 receptor agonist, imetit. The prolactin response to norepinephrine was significantly inhibited by pretreatment with mepyramine, cimetidine or imetit whereas the three histaminergic compounds had no effect on the prolactin response to epinephrine. The findings suggest that the histaminergic system exerts a mediating or permissive action on the norepinephrine-induced stimulation of prolactin secretion, whereas an intact histaminergic system may not be required for catecholamines to stimulate ACTH secretion. The inhibitory effect of imetit on catecholamine-induced release of ACTH may be due to an activation of H3 receptors located presynaptically on non-histaminergic neurons, e.g. aminergic neurons. The study further indicates an important role of histamine in the neuroendocrine regulation of prolactin secretion.
Willems
E
E
Department of Medical Physiology, Division of Endocrinology and Metabolism, The Panum Institute, Copenhagen, Denmarkk.
Knigge
U
U
Jorgensen
H
H
Kjaer
A
A
Warberg
J
J
D000324:Adrenocorticotropic Hormone / Q000378:metabolism*; D000368:Aged; D000818:Animals; D002395:Catecholamines / Q000494:pharmacology*; D004837:Epinephrine / Q000494:pharmacology; D006634:Histamine H1 Antagonists / Q000494:pharmacology*; D006635:Histamine H2 Antagonists / Q000494:pharmacology*; D006801:Humans; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D017729:Presynaptic Terminals / Q000187:drug effects; D011388:Prolactin / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D018100:Receptors, Histamine H3 / Q000502:physiology*; D013569:Synapses / Q000187:drug effects
D002395:Catecholamines; D006634:Histamine H1 Antagonists; D006635:Histamine H2 Antagonists; D018100:Receptors, Histamine H3; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D009638:Norepinephrine; D004837:Epinephrine