Inhibition of vagally mediated gastric acid secretion by activation of central prostanoid EP3 receptors in urethane‐anaesthetized rats

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) reduce...

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Bibliographic Details
Published in:British journal of pharmacology 1996-02, Vol.117 (4), p.653-656
Main Authors: Yokotani, Kunihiko, Okuma, Yasunobu, Osumi, Yoshitsugu
Format: Article
Language:English
Subjects:
Anesthetics, Intravenous
Animals
Biological and medical sciences
Central nervous system
Dinoprostone - analogs & derivatives
Dinoprostone - pharmacology
Electric Stimulation
EP3 receptor
Fundamental and applied biological sciences. Psychology
Gastric Acid - metabolism
gastric acid secretion
Male
Misoprostol - pharmacology
Prostaglandins. Arachidonic acid metabolites
Rats
Rats, Wistar
Receptors, Prostaglandin E - agonists
Receptors, Prostaglandin E - physiology
Urethane
Vagus Nerve - drug effects
Vagus Nerve - physiology
Vertebrates: endocrinology
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Summary: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.
ISSN:0007-1188
1476-5381
DOI:10.1111/j.1476-5381.1996.tb15240.x