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Changes in nitric oxide production with lesion development in the gastric mucosa of rats with water immersion restraint stress.

Keiichiro Nishida, Yasutoshi Ohta, Isao Ishiguro

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Abstract

In rats with gastric mucosal lesions induced by water immersion restraint (WIR) stress over a 6 h period, increases in the serum and gastric mucosal concentrations of nitrite/nitrate, the breakdown products of NO, occurred with a drastic increase in inducible NO synthase (iNOS) activity in the gastric mucosa. Pretreatment with aminoguanidine (100 mg/kg), a relatively selective iNOS inhibitor, attenuated not only gastric mucosal lesion development, but also increases in serum and gastric mucosal nitrite/nitrate concentrations with inhibition of increased gastric mucosal iNOS activity in rats with 6 h of WIR stress. A good positive correlation between either serum or gastric mucosal nitrite/nitrate concentration and gastric mucosal iNOS activity in all rats used (r = 0.741 or 0.842, respectively, p < 0.001) was found. These results suggest that in WIR-stressed rats, an increase in NO production via iNOS in the gastric mucosa could contribute to gastric mucosal lesion development.

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What this paper is about

In rats with gastric mucosal lesions induced by water immersion restraint (WIR) stress over a 6 h period, increases in the serum and gastric mucosal concentrations of nitrite/nitrate, the breakdown products of NO, occurred with a drastic increase in inducible NO synthase (iNOS) activity in the gastric mucosa. Pretreatment with aminoguanidine (100 mg/kg), a relatively selective iNOS inhibitor, attenuated not only gastric mucosal lesion development, but also increases in serum and gastric mucosal nitrite/nitrate concentrations with inhibition of increased gastric mucosal iNOS activity in rats with 6 h of WIR stress. A good positive correlation between either serum or gastric mucosal nitrite/nitrate concentration and gastric mucosal iNOS activity in all rats used (r = 0.741 or 0.842, respectively, p < 0.001) was found. These results suggest that in WIR-stressed rats, an increase in NO production via iNOS in the gastric mucosa could contribute to gastric mucosal lesion development.

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Available abstract

In rats with gastric mucosal lesions induced by water immersion restraint (WIR) stress over a 6 h period, increases in the serum and gastric mucosal concentrations of nitrite/nitrate, the breakdown products of NO, occurred with a drastic increase in inducible NO synthase (iNOS) activity in the gastric mucosa. Pretreatment with aminoguanidine (100 mg/kg), a relatively selective iNOS inhibitor, attenuated not only gastric mucosal lesion development, but also increases in serum and gastric mucosal nitrite/nitrate concentrations with inhibition of increased gastric mucosal iNOS activity in rats with 6 h of WIR stress. A good positive correlation between either serum or gastric mucosal nitrite/nitrate concentration and gastric mucosal iNOS activity in all rats used (r = 0.741 or 0.842, respectively, p < 0.001) was found. These results suggest that in WIR-stressed rats, an increase in NO production via iNOS in the gastric mucosa could contribute to gastric mucosal lesion development.

Key concepts: Gastric mucosa, Nitrite, Nitric oxide, Lesion, Nitric oxide synthase, Chemistry, Nitrate, Internal medicine

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Changes in nitric oxide production with lesion development in the gastric mucosa of rats with water immersion restraint stress. — Research Paper | ScholarLens