Catecholamine receptors involved in the inhibitory effects of dopamine on vagally stimulated gastric acid secretion and mucosal blood flow in rats.

The mechanisms of inhibitory effects of dopamine on the vagally stimulated gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized rats with a gastric fistula. Intravenous infusion of dopamine significantly reduced both gastric acid secretion and MBF. The inhibitory effect of dopamine on the vagally stimulated gastric acid secretion was not attenuated by sulpiride, metoclopramide or domperidone. Haloperidol abolished the inhibitory effect of dopamine on the acid secretion; it also abolished the inhibitory effect of norepinephrine on the vagally stimulated acid secretion. The inhibitory effect of dopamine on the acid secretion was abolished by phentolamine and yohimbine but not by propranolol or prazosin. Dopamine-induced reduction in the vagally stimulated gastric MBF was abolished by haloperidol and was partially antagonized by sulpiride or metoclopramide. In addition, the dopamine-induced reduction in the MBF was abolished by phentolamine and prazosin and was partially antagonized by yohimbine. These results indicate that the inhibitory effect of dopamine on the vagally stimulated gastric acid secretion is mediated by alpha-2 adrenoceptor mechanisms and that the inhibitory effect of dopamine on the MBF is, at least in part, mediated by alpha-1 adrenoceptor mechanisms. The authors did not obtain evidence for the existence of dopamine receptor-mediated mechanisms.