Paradoxical effects of gastrin releasing peptide on gastrin release and gastric secretion in the rat

1986 ◽  
Vol 21 (6) ◽  
pp. 573-578 ◽  
Author(s):  
Atsushi Takagi ◽  
Motoyuki Moriga ◽  
Hiroaki Narusawa ◽  
Haruto Uchino ◽  
Mitsuru Aoo
1979 ◽  
Vol 9 (3) ◽  
pp. 197-202
Author(s):  
Yukio Nagamachi ◽  
Akira Taniguchi ◽  
Nobuo Ogata ◽  
Takuji Nakamura

1999 ◽  
Vol 276 (1) ◽  
pp. G227-G237 ◽  
Author(s):  
Paul E. Squires ◽  
R. Mark Meloche ◽  
Alison M. J. Buchan

Amplification of mRNA from a human antral cell culture preparation demonstrated the presence of two receptors of the bombesin and gastrin-releasing peptide family, GRPR-1 and BRS-3. Single cell microfluorometry demonstrated that most cells that exhibited bombesin-evoked changes in intracellular Ca2+ concentration were gastrin immunoreactive, indicating that antral G cells express the GRPR subtype. There were two components to the intracellular Ca2+ response: an initial nitrendipine-insensitive mobilization followed by a sustained phase that was inhibited by removal of extracellular Ca2+ and 20 mM caffeine and was partially inhibited by 10 μM nitrendipine. Preexposure of cells to thapsigargin and caffeine prevented the response to bombesin, indicating activation of inositol 1,4,5-trisphosphate (IP3)-sensitive stores. Gastrin release could be partially reversed by removal of extracellular Ca2+ and blockade of L-type voltage-dependent Ca2+ channels, indicating that a component of the secretory response to bombesin was dependent on Ca2+ influx. These data demonstrated that bombesin-stimulated gastrin release from human antral G cells resulted from activation of GRPRs and involved both release of intracellular Ca2+ and influx of extracellular Ca2+through a combination of L-type voltage-gated and IP3-gated Ca2+ channels.


Gut ◽  
1992 ◽  
Vol 33 (5) ◽  
pp. 601-603 ◽  
Author(s):  
K Beardshall ◽  
S Moss ◽  
J Gill ◽  
S Levi ◽  
P Ghosh ◽  
...  

1996 ◽  
Vol 271 (5) ◽  
pp. G799-G804 ◽  
Author(s):  
Y. Takehara ◽  
K. Sumii ◽  
A. Tari ◽  
M. Yoshihara ◽  
M. Sumii ◽  
...  

To investigate the physiological role of endogenous gastrin-releasing peptide (GRP) in regulating the release of gastrin, we evaluated the response of intragastric pH, gastrin, and GRP after omeprazole treatment in rats. 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) were observed after the administration of 100 mg/kg omeprazole. The antral content of GRP was significantly decreased 12 h after omeprazole administration and thereafter gradually returned to control levels. Peak values for intragastric pH and plasma GRP were observed 3 h after omeprazole administration and before the peak of serum gastrin. The bombesin antagonist [D-Phe6]-bombesin-(6,13)-methyl ester significantly inhibited gastrin release after omeprazole treatment (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.


1997 ◽  
Vol 69 (1) ◽  
pp. 33-40 ◽  
Author(s):  
N Weigert ◽  
Y.Y Li ◽  
R.R Schick ◽  
D.H Coy ◽  
M Classen ◽  
...  

1982 ◽  
Vol 12 (2) ◽  
Author(s):  
Hans C. Dollinger ◽  
Sotos Raptis ◽  
Bärbel Grebe ◽  
Roland Müller

1957 ◽  
Vol 190 (3) ◽  
pp. 396-402 ◽  
Author(s):  
Herbert B. Greenlee ◽  
Enrique H. Longhi ◽  
Jose Delgadillo Guerrero ◽  
Thomas S. Nelsen ◽  
Abdul Latif El-Bedri ◽  
...  

In dogs prepared with both a vagus denervated Heidenhain pouch and a total pancreatic fistula, the intravenous injection of pancreatic secretin (Lilly) produced a profuse secretion of pancreatic juice and a simultaneous marked inhibition of gastric secretion. In dogs prepared with an isolated antrum pouch and a Heidenhain pouch the gastric secretion induced by the instillation of food in the antrum pouch was completely inhibited by the intravenous injection of pancreatic secretin. On the other hand, the intravenous injection of pancreatic secretin had little or no effect on the secretion of gastric juice produced by insulin hypoglycemia or by the injection of histamine. It is suggested that pancreatic secretin may represent the mechanism by means of which acid food in the duodenum inhibits gastric secretion. It is probable that this inhibition is caused by prevention of gastrin release from the antrum rather than to a depressant effect on the parietal cells.


1977 ◽  
Vol 122 (3) ◽  
pp. 209-222 ◽  
Author(s):  
TSUNEO SHIRATORI ◽  
TOSHIHIKO OKABAYASHI ◽  
MASATO NISHIGORI ◽  
RITSURO SAKURAI ◽  
YOSHIHIRO SHIMANO

1977 ◽  
Vol 233 (3) ◽  
pp. E170
Author(s):  
S J Konturek ◽  
J Tasler ◽  
M Cieszkowski ◽  
M Dobrzańska ◽  
E Wünsch

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