RT Journal Article SR Electronic T1 Effects of the sympathetic nervous system on bethanechol-induced elevation of gastric acid secretion and mucosal blood flow in rats. JF Journal of Pharmacology and Experimental Therapeutics JO J Pharmacol Exp Ther FD American Society for Pharmacology and Experimental Therapeutics SP 478 OP 483 VO 227 IS 2 A1 K Yokotani A1 I Muramatsu A1 M Fujiwara YR 1983 UL http://jpet.aspetjournals.org/content/227/2/478.abstract AB Effects of stimulation of the sympathetic nervous system on the bethanechol-induced increase in gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized, gastric fistula rats. The gastric acid secretion and MBF were increased by i.v. infusion of a supramaximal dose of bethanechol (10.0 micrograms/kg/min). The bethanechol-induced gastric acid secretion was abolished by administration of atropine (0.1 mg/kg i.v.), but was not influenced by hexamethonium (2.0 mg/kg i.v.) in the dose which abolished the gastric acid secretion induced by vagus nerve stimulation. Stimulation of the splanchnic postganglionic (SP) nerve or infusion of norepinephrine was carried out under the steady, increased state of acid secretion and MBF. Stimulation of the SP nerve significantly reduced the gastric acid secretion but the MBF was little affected. Thus, the delta MBF/delta H+ ratio was significantly increased during this stimulation. Intravenous infusion of norepinephrine also reduced the acid secretion without affecting the MBF. The delta MBF/delta H+ ratio was also significantly increased during infusion of norepinephrine. Phentolamine, but not propranolol, abolished the inhibitory effects of SP nerve stimulation and infusion of norepinephrine on the gastric acid secretion. These results suggest that the SP nerve acts on the structures peripheral to the postganglionic parasympathetic nerve terminals and directly inhibits the parasympathetically stimulated gastric acid secretion through alpha adrenoceptors, independently of changes in the gastric MBF in rats.