Histamine-induced vasodilations mediated by H1- and H2-receptors in isolated rat common carotid arteries.

Using the cannula inserting method, the vasodilatory effects of histamine were analysed employing selective histamine H1- and H2-receptor agonists and antagonists in isolated, perfused rat common carotid arterial preparations which were preconstricted by a continuous infusion of phenylephrine with propranolol. Histamine, 2-pyridylethylamine (2-PEA) (a selective H1-agonist) and dimaprit (a selective H2-agonist) produced a vasodilation in a dose-related manner. The order of potency was histamine greater than dimaprit greater than 2-PEA. Histamine-induced dilations were significantly inhibited by either diphenhydramine (a selective H1-antagonist) or cimetidine (a selective H2-antagonist). 2-PEA-induced dilations were significantly inhibited by diphenhydramine but not by cimetidine. Dimaprit-induced dilations were significantly blocked by cimetidine but not by diphenhydramine. ACh-, histamine-, 2-PEA- and dimaprit-induced dilations were significantly suppressed by removal of the endothelium. From these results, it is concluded that (1) isolated rat common carotid arteries have both H1- and H2-receptors, (2) there are few vasoconstrictory H1-receptors, (3) both H1- and H2-receptors mediate only vasodilation but not vasoconstriction, and (4) EDRF from the endothelium might participate in histamine-induced vasodilation via not only H1- but also H2-receptors.