Possible role for oxygen free radicals in the regulation of renal nitric oxide synthesis and blood flow

Background This study examines the hypothesis that oxygen radicals down-regulate renal nitric oxide synthesis and contribute to renal vasoconstriction after hemorrhage/reperfusion injury. Methods Arterial pressure and renal artery blood flow were measured in anesthetized rats subjected to sham or hemorrhage (30 nun Hg for 30 minutes) followed by blood reperfusion without or with superoxide dismutase, an oxygen radical scavenger. Animals were sequentially injected with 10 mg/kg NG-nitro-l-arginine methyl ester (l-NAME), a nitric oxide synthase inhibitor, and 200 mg/kg and 400 mg/kg l-arginine, a nitric oxide precursor. Results The l-NAME treatment increased arterial pressure and decreased renal artery blood flow whereas l-arginine decreased arterial pressure and decreased renal blood flow in the sham animals. Hemorrhage/reperfusion injury attenuated the pressure and renal blood flow changes following l-NAME and l-argininene treatment, which was reversed by superoxide dismutase. Conclusions These data suggest that oxygen radicals contribute to the regulation of renal nitric oxide synthesis, contributing to renal artery vasoconstriction following hemorrhage/reperfusion injury.