A central site of dopamine agonist action to modify gastric secretion in the rat.

2-Di-n-propylamino-5,6-dihydroxytetralin (tetralin) administered subcutaneously (6.25-25 micrograms/kg s.c.) or into the cerebral ventricles (i.c.v. 0.5-10 micrograms) dose-dependently reduced the volume and acid concentration of gastric secretion collected from rats having chronically implanted gastric and intracerebral cannulas. Apomorphine or dopamine given i.c.v. also reduced gastric secretory volume and acid concentration. Tetralin-induced reductions (s.c. or i.c.v.) in gastric acid concentrations were antagonised by the dopamine antagonists metoclopramide, sulpiride or haloperidol and by the alpha 2-adrenoceptor antagonist yohimbine given systemically or i.c.v. The alpha 2-adrenoceptor antagonist idazoxan or the beta-adrenoceptor antagonist propranolol (i.c.v.) also antagonised the tetralin-induced (i.c.v.) reduction in gastric acid concentration. In contrast, the reduction in gastric secretory volume effected by centrally or peripherally administered tetralin could only be antagonised by propranolol. Previous observations that apomorphine can reduce gastric secretory volume and acid concentration are thus extended to 2-di-n-propylamino-5,6-dihydroxytetralin. Both agents reduce gastric secretory volume via an action on beta-adrenoceptors, and reduce gastric acid concentration via dopamine receptors, with alpha 2-adrenoceptor and, more speculatively, beta-adrenoceptor mechanisms contributing to the effect of the tetralin compound. These actions may be mediated, at least in part, via central mechanisms.