scholarly journals Bombesin Antagonist

2020 ◽  
Author(s):  
Keyword(s):  
2010 ◽  
Vol 38 (1) ◽  
pp. 97-107 ◽  
Author(s):  
Rosalba Mansi ◽  
Xuejuan Wang ◽  
Flavio Forrer ◽  
Beatrice Waser ◽  
Renzo Cescato ◽  
...  
Keyword(s):  

2011 ◽  
Vol 52 (12) ◽  
pp. 1970-1978 ◽  
Author(s):  
K. Abiraj ◽  
R. Mansi ◽  
M.-L. Tamma ◽  
M. Fani ◽  
F. Forrer ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e81932 ◽  
Author(s):  
Zohreh Varasteh ◽  
Ola Åberg ◽  
Irina Velikyan ◽  
Gunnar Lindeberg ◽  
Jens Sörensen ◽  
...  

2010 ◽  
Vol 37 (6) ◽  
pp. 725-726 ◽  
Author(s):  
Charles Jeffrey Smith ◽  
Prasant K. Nanda ◽  
Stephanie Lane ◽  
Gary L. Sieckman ◽  
Timothy J. Hoffman ◽  
...  

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.


2013 ◽  
Vol 24 (7) ◽  
pp. 1144-1153 ◽  
Author(s):  
Zohreh Varasteh ◽  
Irina Velikyan ◽  
Gunnar Lindeberg ◽  
Jens Sörensen ◽  
Mats Larhed ◽  
...  

Peptides ◽  
1992 ◽  
pp. 225-226
Author(s):  
J. A. Malikayil ◽  
J. Vincent Edwards ◽  
Larry R. McLean
Keyword(s):  
2D Nmr ◽  

1996 ◽  
Vol 271 (6) ◽  
pp. R1584-R1593 ◽  
Author(s):  
E. Yoshida-Yoneda ◽  
T. J. O-Lee ◽  
J. Y. Wei ◽  
S. R. Vigna ◽  
Y. Tache

Bombesin's influence on gastric vagal afferent discharge (GVAD) was studied in urethan-anesthetized rats. Vehicle and peptides were injected intravenously at 30-min intervals. Cholecystokinin (CCK; 300 pmol) and bombesin (300 pmol) increased ongoing multiunit GVAD by 153 +/- 59 and 162 +/- 37%, respectively; similar increases were induced by a second injection of bombesin and CCK. The bombesin antagonist, ICI-216140, prevented bombesin-induced increase in GVAD, whereas the CCK response was not influenced. The CCK-A receptor antagonist devazepide reduced the activation of GVAD induced by bombesin from 107 +/- 11 to 63 +/- 6%, while abolishing the CCK response. Devazepide given alone or in combination with ICI-216140 did not modify gastric distension (3 ml)-induced increase in GVAD. Of 22 single units that were activated by gastric load (4 ml), 17 and 20 units responded also to bombesin (620 pmol) and CCK (870 pmol), respectively. Of the nine units that did not respond to gastric load, eight had an increase in GVAD induced by both bombesin and CCK. There was no specific binding of 125I-labeled [Tyr4]bombesin on cervical vagus, either intact or 24 h after ligation. These data suggest that intravenous bombesin-induced stimulation of GVAD is indirect and initially mediated through specific receptor activation influencing gastric smooth muscle and the release of CCK.


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