Evidence that endogenous grp in rat stomach mediates omeprazole
induced hypergastrinemia.
Takehara, Yoshihiko, Koji Sumii, Akira Tari, Masaharu Yoshihara,
Masaharu Sumii, Ken Haruma, Goro Kajiyama, S. Vincent Wu, and John H.
Walsh.
First Department of Internal Medicine, Hiroshima University School
of Medicine, Hiroshima, Japan, Center for Ulcer Research and
Education, West Los Angeles Veterans Administration Center, and UCLA
School of Medicine, Los Angeles, California
APStracts 3:0104G, 1996.
To investigate the physiologic role of endogenous gastrin-releasing
peptide (GRP) in regulating the release of gastrin, we evaluated the
response of intragastric pH, gastrin, and GRP following the
omeprazole treatment in rat. A significant elevation of the plasma
level of GRP (p<0.01) and a significant reduction of the antral
content of GRP (p<0.05) was observed following the
administration of omeprazole, 100 mg/kg. The antral content of GRP
was significantly decreased 12 h following omeprazole administration,
and thereafter gradually returned to control levels. Peak values for
intragastric pH and plasma GRP were observed 3 h following omeprazole
administration and before the peak of serum gastrin. Bombesin
antagonist, [D-Phe6]bombesin(6-13)-methyl-ester (BME), inhibited
gastrin release following omeprazole treatment significantly
(p<0.05). These observations indicate that omeprazole-induced
inhibition of acid secretion stimulates the release of GRP, and
suggest that the secretion of GRP induced by omeprazole may stimulate
the secretion of gastrin, at least in the early phase.
Received 10 October 1995; accepted in final form 22 April 1996.
APS Manuscript Number G441-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 May 96