Selective and competitive histamine H2-receptor blocking effect of famotidine on the blood pressure response in dogs and the acid secretory response in rats.

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Famotidine has been already demonstrated to be a competitive H2-receptor antagonist in the stomachs of dogs and cats. The present experiments were carried out to examine the effects of famotidine on changes in blood pressure induced by dimaprit and several other agonists in vagotomized, anesthetized dogs and on changes in gastric acid secretion induced by histamine in stomach-perfused, anesthetized rats. Famotidine caused a parallel displacement of the dimaprit dose-response curve to the right with a DR10 value of 0.059 μmol/kg, indicating that famotidine is 166 times more potent than cimetidine in vascular H2-blocking activity. On the contrary, famotidine did not affect the depressor responses to 2-pyridylethylamine and histamine that were antagonized by mepyramine. The histamine dose-response curve was displaced to the right more markedly after simultaneous administration of mepyramine and famotidine than after mepyramine alone. The effects of methacholine, phenylephrine and isoproterenol on blood pressure were not influenced by famotidine in doses up to 720 nmol/kg. In rats, famotidine also caused a parallel displacement of the acid dose-response curve to histamine to the right with a DR3 value of 24 μmol/kg/hr in stomach-perfused rats anesthetized with pentobarbital, exhibiting a potency 108 times greater than that of cimetidine. Analysis of the acid dose-response curve with the Edie-Hofstee transformation showed that famotidine, like cimetidine, was a competitive H2-receptor antagonist.
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Selective and competitive histamine H2-receptor blocking effect of famotidine on the blood pressure response in dogs and the acid secretory response in rats.

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