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
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.