Studies with specific agonists and antagonists of the role of histamine H1- and H2-receptor activation in the pathogenesis of gastric lesions in rats.

Although the factors involved in the induction of gastric pathology have long been studied, the exact roles of the two histamine receptors in this process are still obscure. The aim of this study was to evaluate the consequences of the activation of histamine H1- and/or H2-receptors in the pathogenesis of gastric damage and antagonism of these pathological developments by specific antagonists. The following agents were used: histamine as H1- and H2H2-agonist; 2-pyridylethylamine (PEA) and mepyramine as H1-agonist and antagonist; dimaprit and ranitidine as H2-agonist and antagonist. Intravenous administration of the agonists caused definite gastric damage in rats. Both the antagonists inhibited histamine-induced gastric lesions, but the PEA and dimaprit-induced erosions could be prevented only by giving the specific H1- or H2-antagonist. In conclusion, activation of either H1- or H2-receptors can play a crucial role in the pathogenesis of histamine-induced gastric damage in rats.