Vanillyl nonanoate protects rat gastric mucosa from ethanol-induced injury through a mechanism involving calcitonin gene-related peptide

2011 ◽  
Vol 666 (1-3) ◽  
pp. 211-217 ◽  
Author(s):  
Xiu-Ju Luo ◽  
Nian-Sheng Li ◽  
Yi-Shuai Zhang ◽  
Bin Liu ◽  
Zhi-Chun Yang ◽  
...  
1995 ◽  
Vol 58 (4) ◽  
pp. 421-424 ◽  
Author(s):  
Craig A. Miller ◽  
Masanobu Nakashima ◽  
George K. Gittes ◽  
Halle T. Debas

Peptides ◽  
2002 ◽  
Vol 23 (5) ◽  
pp. 955-966 ◽  
Author(s):  
Kousaku Kawashima ◽  
Shunji Ishihara ◽  
Mohammad Azharul Karim Rumi ◽  
Nobuyuki Moriyama ◽  
Hideaki Kazumori ◽  
...  

1995 ◽  
Vol 73 (7) ◽  
pp. 991-994 ◽  
Author(s):  
P. Holzer ◽  
Ch. Wachter ◽  
M. Jocič ◽  
I. Th. Lippe ◽  
A. Heinemann ◽  
...  

Calcitonin gene related peptide (CGRP) is the major mediator of afferent nerve mediated vasodilatation in the gastric mucosa and skin of the rat. Since receptors for CGRP occur on both the vascular endothelium and smooth muscle, it is conceivable that the vascular actions of CGRP involve multiple mechanisms. The vasodilator effect of rat CGRP-α in the rat gastric mucosa is indeed inhibited by blockade of nitric oxide (NO) synthesis, as is the gastric mucosal hyperemia in response to gastric acid challenge, which is mediated by CGRP release from afferent nerve fibres. In contrast, the vasodilator response to rat CGRP-α in the rat hind paw and the CGRP-mediated vasodilatation evoked by antidromic stimulation of afferent nerve fibres do not depend on the formation of NO. These data indicate that NO plays regionally different roles in the local vasodilator action of CGRP. NO is a secondary vasorelaxant messenger of CGRP in the gastric, but not in the cutaneous, microcirculation. However, this L-arginine-derived autacoid may have a role in the irritant-induced CGRP release from afferent vasodilator fibres in the skin.Key words: calcitonin gene related peptide, nitric oxide, microcirculation, gastric mucosa, skin, afferent nerve fibres, neurogenic vasodilatation.


Digestion ◽  
1999 ◽  
Vol 60 (4) ◽  
pp. 338-343 ◽  
Author(s):  
Norio Tani ◽  
Masayuki Miyazawa ◽  
Takeshi Miwa ◽  
Masahiro Shibata ◽  
Tetsuaki Yamaura

1991 ◽  
Vol 261 (4) ◽  
pp. G657-G661 ◽  
Author(s):  
D. S. Li ◽  
H. E. Raybould ◽  
E. Quintero ◽  
P. H. Guth

Stimulation of sensory neurons in the rat stomach by intragastric capsaicin leads to a marked rise in gastric mucosal blood flow (GMBF). The gastric mucosa, in particular submucosal blood vessels, is densely innervated by afferent neurons containing peptides, of which calcitonin gene-related peptide (CGRP) is the most potent vasodilator. Using selective ablation of either the vagal or spinal sensory innervation to the stomach by perineural application of capsaicin, and by intra-arterial infusion of the CGRP receptor antagonist hCGRP-(8-37) close to the stomach, we investigated 1) the origin (vagal or spinal) of the sensory neurons and 2) whether CGRP mediates this hyperemic response. Perivagal application of capsaicin to the rat 10-20 days before experiments had no effect on the hyperemic response to intragastric capsaicin. In contrast, periceliac application of capsaicin significantly reduced this response by 60%. Intra-arterial infusion of CGRP (20 pmol/min) close to the stomach produced a marked rise in GMBF and this was completely blocked by hCGRP-(8-37) (500 pmol/min). intra-arterial infusion of hCGRP-(8-37) or its vehicle, bovine serum albumin, had no significant effect on basal GMBF. However, the increment in GMBF in response to intragastric capsaicin was significantly attenuated by 79%. We conclude that 1) spinal sensory neurons innervating the gastric mucosa partially mediate the increase in GMBF induced by intragastric capsaicin and 2) CGRP is the major vasodilator released by these fibers.


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