Central and peripheral effects of prostaglandin E2 and enprostil on gastric acid secretion in the rat

Sautereau, Denis; Chicau-Chovet, Maria; Tsocas, Annick; Rozé, C

doi:10.1016/0014-2999(91)90538-2

Cited by 5 publications

(2 citation statements)

References 13 publications

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“…Prostaglandins are produced in the central nervous system of mammals (Wolfe, 1982) and are implicated in central regulation of a variety of functions, including body temperature (Coceani et al, 1988), hypothalamic and pituitary hormone release (Behrman, 1979), some behavioural activities (Johnson et al, 1993) and the control of gastric functions (Saperas et al, 1991;Sautereau et al, 1991). Receptors activated by prostaglandin E2 (PGE2) are pharmacologically divided into at least three subtypes (EPI,EP2 and EP3).…”

Section: Introductionmentioning

confidence: 99%

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

Yokotani¹,

Okuma²,

Osumi³

1996

British J Pharmacology

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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/EPj 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-cotrinor 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 EP, 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 > > 1 7-phenyl-co-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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Section: Introductionmentioning

confidence: 99%

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

Yokotani¹,

Okuma²,

Osumi³

1996

British J Pharmacology

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“…These cytokines have been reported to stimulate COX-2 expression resulting in increases in PGE 2 synthesis (25,26). PGE 2 is well known as a potent inhibitor of gastric acid secretion (9,27). In a human study, administration of PGE 2 was shown to reduce gastric juice H ‡ output (28).…”

Section: Discussionmentioning

confidence: 97%

Effects of Cyclooxygenase-2 Inhibitor on Gastric Acid Secretion in Helicobacter pylori-infected C57BL/6 Mice

Xiao¹,

Furuta²,

Takashima³

et al. 2001

Scandinavian Journal of Gastroenterology

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Characterization of the mechanisms involved in the gastric antisecretory effect of TLQP-21, a vgf-derived peptide, in rats

et al. 2010

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TLQP-21, a vgf-derived peptide modulates gastric emptying and prevents ethanol-induced gastric lesions in rats. However, it remains to be studied whether or not TLQP-21 affects gastric acid secretion. In this study, we evaluated the effects of central (0.8-8 nmol/rat) or peripheral (48-240 nmol/kg, intraperitoneally) TLQP-21 administration on gastric acid secretion in pylorus-ligated rats. The mechanisms involved in such activity were also examined. Central TLQP-21 injection significantly reduced gastric acid volume and dose-dependently inhibited total acid output (ED(50) = 2.71 nmol), while peripheral TLQP-21 administration had no effect. The TLQP-21 antisecretory activity was prevented by cysteamine (300 mg/kg, subcutaneously), a depletor of somatostatin, by indomethacin (0.25 mg/rat, intracerebroventricularly), a non-selective cyclooxygenase inhibitor, and by functional ablation of sensory nerves by capsaicin. We conclude that TLQP-21 could be considered a new member of the large group of regulatory peptides affecting gastric acid secretion. The central inhibitory effect of TLQP-21 on gastric acid secretion is mediated by endogenous somatostatin and prostaglandins and requires the integrity of sensory nerve fibres.

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Central and peripheral effects of prostaglandin E2 and enprostil on gastric acid secretion in the rat

Cited by 5 publications

References 13 publications

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

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

Effects of Cyclooxygenase-2 Inhibitor on Gastric Acid Secretion in Helicobacter pylori-infected C57BL/6 Mice

Characterization of the mechanisms involved in the gastric antisecretory effect of TLQP-21, a vgf-derived peptide, in rats

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Central and peripheral effects of prostaglandin E2 and enprostil on gastric acid secretion in the rat

Cited by 5 publications

References 13 publications

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

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

Effects of Cyclooxygenase-2 Inhibitor on Gastric Acid Secretion in Helicobacter pylori-infected C57BL/6 Mice

Characterization of the mechanisms involved in the gastric antisecretory effect of TLQP-21, a vgf-derived peptide, in rats

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

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