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

Abstract

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.

Functional Analysis Of Histamine Receptor Subtypes Involved In Endothelium‐Mediated Relaxation Of The Human Uterine Artery

“…, who described that, in human cranial arteries, mRNA encoding H 1 and H 2 receptors is detectable 20 . In agreement with our results obtained with human arteries, in the isolated rat common carotid artery, both H 1 and H 2 receptors are involved in the mechanisms of histamine‐induced relaxation 21 . In porcine endothelial cells, histamine‐evoked formation of nitric oxide was shown to be mediated by the H 2 receptor 22 .…”

“…20 In agreement with our results obtained with human arteries, in the isolated rat common carotid artery, both H1 and H2 receptors are involved in the mechanisms of histamine-induced relaxation. 21 In porcine endothelial cells, histamine-evoked formation of nitric oxide was shown to be mediated by the H2 receptor. 22 Because the selective H3 receptor agonist imetit failed to initiate any relaxation, our data suggest that the H3 receptor is not expressed functionally in these types of vessels.…”

Migraine and Function of the Immune System: A Meta-Analysis of Clinical Literature Published Between 1966 and 1999

“…Histamine challenge in migraine patients and healthy volunteers, respectively, induced a migraine attack and headache (25–27). Histamine is a potent vasoactive compound (28–35), and since the headache of a migraine attack has been attributed to cerebrovascular vasodilation (36–39), histamine may be a candidate mediator for vascular changes observed during a migraine attack. There is evidence that the vascular effects of histamine are at least partially mediated by nitric oxide (NO) (40), a gaseous molecule with a potential important role in development of migraine.…”