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Inhibition of vagally mediated gastric acid secretion by activation of central prostanoid EP 3 receptors in urethane‐anaesthetized rats
Author(s) -
Yokotani Kunihiko,
Okuma Yasunobu,
Osumi Yoshitsugu
Publication year - 1996
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1996.tb15240.x
Subject(s) - prostanoid , receptor , chemistry , endocrinology , secretion , medicine , gastric acid , pharmacology
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 (EP 3 /EP 2 receptor agonist) and sulprostone (EP 3 /EP 1 receptor agonist) reduced vagally mediated gastric acid secretion in a dose‐dependent manner (0.1, 0.3 and 1.0 nmol per animal). Butaprost (EP 2 receptor agonist) (0.3 and 3.0 nmol per animal) was without effect. 17‐Phenyl‐ω‐trinor PGE 2 (EP 1 /EP 3 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 EP 1 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 PGE 2 > > > butaprost. These results suggest that activation of central prostanoid EP 3 receptors induces inhibition of vagally mediated gastric acid secretion in rats.