Endogenous nitric oxide in gastric alkaline response in the rat stomach after damage.

BACKGROUND/AIMS: The gastric mucosa responds to hypertonic NaCl by significantly decreasing acid secretion. This study examined the role of nitric oxide in this phenomenon.

METHODS

A rat stomach was mounted in an ex vivo chamber and perfused with saline; then the potential difference (PD), pH, and acid and/or alkaline responses were measured before and after the application of 1 mol/L NaCl with or without pretreatment with NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO biosynthesis.

RESULTS

A dose of 1 mol/L NaCl caused a reduction in PD, a decrease in basal and histamine-stimulated acid secretion, and an increase in luminal HCO3-. Prior administration of L-NAME did not affect either the PD or the HCO3- response but significantly attenuated the inhibitory effect of 1 mol/L NaCl on acid secretion. This effect of L-NAME was antagonized by the simultaneous administration with L-arginine but not D-arginine. Histamine-stimulated acid secretion in the normal stomach was significantly reduced by the exogenous NO donor nitroprusside but not by L-NAME.

CONCLUSIONS

NO is involved in the mechanism of the gastric alkaline response after damage with 1 mol/L NaCl. Irritation of the gastric mucosa by hypertonic NaCl may release endogenous NO, which in turn inhibits acid secretion and unmasks luminal alkalinization caused by HCO3- flux in the damaged portion.