EVIDENCE THAT ENDOGENOUS GRP IN RAT STOMACH MEDIATES OMEPRAZOLE-INDUCED HYPERGASTRINEMIA

Citation
Y. Takehara et al., EVIDENCE THAT ENDOGENOUS GRP IN RAT STOMACH MEDIATES OMEPRAZOLE-INDUCED HYPERGASTRINEMIA, American journal of physiology: Gastrointestinal and liver physiology, 34(5), 1996, pp. 799-804
Citations number
26
Categorie Soggetti
Physiology
ISSN journal
01931857
Volume
34
Issue
5
Year of publication
1996
Pages
799 - 804
Database
ISI
SICI code
0193-1857(1996)34:5<799:ETEGIR>2.0.ZU;2-3
Abstract
To investigate the physiological role of endogenous gastrin-releasing peptide (GRP) in regulating the release of gastrin, we evaluated the r esponse of intragastric pH, gastrin, and GRP after omeprazole treatmen t in rats. A significant elevation of the plasma level of GRP (P < 0.0 1) and a significant reduction of the antral content of GRP (P < 0.05) were observed after the administration of 100 mg/kg omeprazole. The a ntral content of GRP was significantly decreased 12 h after omeprazole administration and thereafter gradually returned to control levels. P eak values for intragastric pH and plasma GRP were observed 3 h after omeprazole administration and before the peak of serum gastrin. The bo mbesin antagonist [D-Phe(6)]-bombesin-(6,13)-methyl ester significantl y inhibited gastrin release after omeprazole treatment (P < 0.05). The se observations indicate that omeprazole-induced inhibition of acid se cretion stimulates the release of GRP and suggest that the secretion o f GRP induced by omeprazole may stimulate the secretion of gastrin, at least in the early phase.