Résumé
<p><b>AIM</b>To 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.</p><p><b>METHODS</b>Water 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.</p><p><b>RESULTS</b>L-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.</p><p><b>CONCLUSION</b>Endogenous nitric oxide plays an important role in protecting gastric mucosa from stress-induced lesion by inhibiting H+, K(+) -ATPase activity of parietal cells.</p>