Effects of a β₂-Sympathomimetic on Histamine-stimulated Gastric Acid Secretion in Dogs

Abstract

The effect of a selective beta2-adrenoceptor agonist on histamine-stimulated gastric acid secretion was studied in conscious gastric-fistula dogs. A dose-dependent inhibition was found, most pronounced for the lowest doses of histamine. The inhibition was on the volume, whereas the acidity was unchanged. The pulse rate was increased by the beta2-agonist and by histamine. Propranolol prevented the inhibition of acid secretion as well as the increase in pulse rate. Practolol had no effect on the inhibition of acid secretion but reduced the increase in pulse rate. Dose-response experiments with six doses of histamine and two doses of the beta2-agonist showed unchanged calculated maximal response and an increase in D50. It is concluded that the beta2-agonist inhibits histamine-induced acid secretion in the dog, but to a lesser degree that pentagastrin-induced acid secretion, as found in earlier experiments. The inhibition follows competitive kinetics, and beta2-receptors are probably involved. The influence of beta2-sympathomimetics on the mechanism of gastric acid secretion is discussed.

Beta‐adrenergic regulation of cyclic adenosine 3‘,5’ monophosphate accumulation in human gastric epithelial glands. Inhibitory effect of somatostatin

“…In that respect, it is of interest to notice the opposite effects of catecholamines observed in laboratory animals in vitro and in vivo, even within the same species [31-351. For example, Gottrup et al showed that injections of beta agonists decrease gastrin-induced, and to a lesser extent, basal and histamine-induced acid secretion in dogs [31,32,331. Similar inhibitory effects of catecholamines were observed by Canfield et al in rat ir!…”