Evidence for Both Histamine H₁‐ and H₂‐receptors in the Gastric Vasculature of the Cat

1 Experiments have been done to study the gastric vascular response to histamine given intra-arterially in the cat.2 In experiments utilising pump perfusion of the stomach at constant flow rates, rapid intra-arterial injections of histamine elicited dose-dependent vasodilatation. The dose-response curve to histamine was displaced to the right by mepyramine and further to the right by mepyramine plus cimetidine. Cimetidine alone did not displace the histamine dose-response curve. This interaction between histamine and histamine antagonists is very similar to the interaction observed in other vascular beds.3 Intra-arterial infusions of histamine also caused vasodilatation with increased gastric blood flow, measured with an electromagnetic flow probe. Mepyramine reduced the immediate increase in blood flow during each infusion, although responses in the later stages of the infusions were unaltered. Cimetidine had no effect on the immediate response but reduced sustained responses to histamine. Treatment with mepyramine and cimetidine was required to abolish histamine responses.4 Infusions of 2-(2-aminoethyl) pyridine and dimaprit also increased gastric blood flow.5 These results indicate the involvement of both H(1)- and H(2)-receptors in histamine-induced gastric vasodilatation. There appears to be a time-base in the interaction between histamine and vascular histamine receptors; H(1)-receptor responses preceding H(2)-receptor responses.