Protective effect of nitric oxide on gastric mucosa and its relationship to the acid secretion of gastric parietal cells under stress in rats.
- Author:
Guo-Ming LU
1
;
Yu-Mei LI
;
Lian-Jun GUO
;
Ming ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Arginine; metabolism; Gastric Acid; secretion; Gastric Mucosa; metabolism; H(+)-K(+)-Exchanging ATPase; metabolism; Male; Nitric Oxide; metabolism; Nitric Oxide Synthase; metabolism; Oxidative Stress; Parietal Cells, Gastric; metabolism; Rats; Rats, Sprague-Dawley; Stomach Ulcer; metabolism; pathology; Stress, Physiological
- From: Chinese Journal of Applied Physiology 2005;21(3):301-304
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo demonstrate the protective effect of nitric oxide (NO) on gastric mucosa and its relationship to the acid secretion of parietal cells under stress in rats.
METHODSWater immersion-restraint stress (WRS) model in SD rats was performed. The gastric mucosal ulcer index (UI), NO contents in gastric mucosa and H+, K(+) -ATPase activity of parietal cells were measured. The effects of N(G)-nitro-L-arginine methyl ester(L-NAME) and L-arginine (L-Arg) on the H+, K(+)-ATPase activity of parietal cells and stress-induced gastric mucosal lesion were observed.
RESULTSL-NAME pretreatment decreased NO contents in gastric mucosa, activated H+, K(+) -ATPase activity of parietal cells and aggravated gastric mucosal lesion, whereas L-Arg pretreatment increased NO contents, inhibited H+, K(+) -ATPase activity and significantly ameliorated stress-induced gastric mucosal lesion.
CONCLUSIONEndogenous nitric oxide plays an important role in protecting gastric mucosa from stress-induced lesion by inhibiting H+, K(+) -ATPase activity of parietal cells.
