Abstract
The gastric acid secretion induced by infusion of bethanechol (10.0 jig/kg/min) or stimulation of the vagus nerve (0.5 mA, 3 Hz, 0.5 msec) was significantly reduced by SPS, but the gastric mucosal blood flow (MBF) was little affected. The inhibitory effects of SPS on the bethanechol-induced gastric acid secretion was abolished by phentolamine (1.0 and 5.0 mg/kg) and prazosin (0.1 mg/kg), but not influenced by yohimbine (5.0 and 10.0 mg/kg). The inhibitory effects of the SPS on the vagally stimulated gastric acid secretion was abolished by phentolamine (1.0 and 5.0) and yohimbine (3.0 and 5.0), but not influenced by prazosin (0.1 and 5.0). These inhibitory effets of SPS were not influenced by propranolol (5.0 and 10.0 mg/kg). Clonidine (2.0 and 10.0 μg/kg/min i.v.) had no effect on the bethanechol-induced acid secretion, but inhibited the vagally stimulated acid secretion in a dose-dependent manner, and this inhibitory effect was abolished by yohimbine (5.0). It is concluded that the SPS inhibits the parasympathetically stimulated gastric acid secretion through alpha-2 type adrenoceptors on the vagus nerve and through alpha-1 type adrenoceptors on the structures peripheral to vagus nerve terminals in the gastric wall, independently of the MBF.
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