Salvati P, Whittle B J
Eur J Pharmacol. 1983 Apr 22;89(1-2):63-8. doi: 10.1016/0014-2999(83)90608-8.
Gastric vascular responses to histamine and its selective H1- and H2-agonists in vitro were investigated in the isolated vascular-perfused stomach of rabbit and rat. In the rabbit stomach under resting conditions bolus injection of histamine (5-80 nmol) caused a small increase in perfusion pressure (PP). However, during infusion of noradrenaline (1 microM), which elevated vascular tone, histamine (5-80 nmol) caused a dose-dependent biphasic vascular response, an initial increase followed by a fall in PP. Under similar conditions, the H1-agonist 2-pyridyl ethylamine, (2-PE; 50-400 nmol) elevated PP, whereas the H2-agonist dimaprit (80-640 nmol) reduced PP. The H1-antagonist mepyramine (0.25 microM) converted the biphasic response of histamine (5-50 nmol) to a monophasic vasodilation whereas the H2-receptor antagonist, cimetidine (1 microM) converted the biphasic response to a vasoconstriction. Similar responses were observed during conditions of elevated vascular tone induced by vasopressin or angiotensin II. In the rat stomach, histamine and both dimaprit and 2-PE reduced PP during conditions of elevated vascular tone. These findings support the presence of both H1- and H2 receptors in the gastric vasculature of both rat and rabbit; in both species, the H2-response is vasodilation whereas the nature of the H1-response is species dependent.