A study of the vascular and acid‐secretory responses of the rat gastric mucosa to histamine.

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Abstract
The effects of histamine on gastric mucosal blood flow in the presence and absence of gastric acid secretion were studied in the rat. Histamine, in doses greater than those required to stimulate maximal acid secretion, caused a small increase in mucosal blood flow per unit acid output. When acid secretion was inhibited by methyl analogues of prostaglandin E2, histamine reduced arterial blood pressure and gave a dose dependent rise in mucosal blood flow. When acid secretion was inhibited by the histamine H2-receptor antagonists, burimamide and metiamide, histamine still increased mucosal blood flow. The use of H1-receptor antagonists to inhibit the histamine-induced hyperemia was made difficult by their vasodilator actions. The selective histamine H2-receptor agonist, 4-methyl histamine, had no effect on arterial blood pressure in doses which stimulated acid secretion. The increase in mucosal blood flow which accompanied the stimulation of acid secretion was inhibited by the anti-secretory prostaglandins and H2-receptor antagonists. The selective histamine H1-receptor agonist, 2-pyridylethylamine, had no effect on acid output but increased resting mucosal blood flow. Histamine H2-receptors, primarily concerned with acid secretion, and H1-receptors concerned with vasodilatation are both present in the rat gastric mucosa.