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  • Title: Inhibition of vagally mediated gastric acid secretion by activation of central prostanoid EP3 receptors in urethane-anaesthetized rats.
    Author: Yokotani K, Okuma Y, Osumi Y.
    Journal: Br J Pharmacol; 1996 Feb; 117(4):653-6. PubMed ID: 8646410.
    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-omega- 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 > or = sulprostone > > 17-phenyl-omega-trinor PGE2 > > > butaprost. These results suggest that activation of central prostanoid EP3 receptors induces inhibition of vagally mediated gastric acid secretion in rats.
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