K. Yokotani, Y. Okuma, Y. Osumi
Feb 1, 1996
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Journal
British Journal of Pharmacology
Abstract
1 We studied the effects of intracerebroventricular (i.c.v.) administration of prostanoid EP receptor ligands on vagally stimulated gastric acid secretion in rats anaesthetized with urethane. 2 Administration of misoprostol (EP3/EP2 receptor agonist) and sulprostone (EP3/EP1 receptor agonist) reduced vagally mediated gastric acid secretion in a dose‐dependent manner (0.1, 0.3 and 1.0 nmol per animal). Butaprost (EP2 receptor agonist) (0.3 and 3.0 nmol per animal) was without effect. 17‐Phenyl‐ω‐trinor PGE2 (EP1/EP3 receptor agonist) attenuated vagally mediated gastric acid secretion only at its highest dose (1.0 nmol per animal); this antisecretory effect was not prevented by pretreatment with SC‐19220 (selective EP1 receptor antagonist) (20 nmol per animal, i.c.v.). 3 The potency of these test agents in attenuation of vagally mediated gastric acid secretion was as follows: misoprostol ≥ sulprostone ≫ 17‐phenyl‐ω‐trinor PGE2> > > butaprost. These results suggest that activation of central prostanoid EP3 receptors induces inhibition of vagally mediated gastric acid secretion in rats.