SODIUM-AZIDE PROTECTS AGAINST ISCHEMIA-INDUCED ACUTE-RENAL-FAILURE INRATS

Sodium azide (AZ) is a nitrovasodilator with diverse biochemical prope rties. We found that low doses of AZ led to a profound protective effe ct against postischemic, acute renal failure (ARF) in rats. AZ, given at 250 mug/kg iv, before 25 min of renal artery occlusion (RAO) and ag ain before reperfusion, conferred almost complete protection against l oss of kidney function determined 18 h after RAO. The effect of AZ was evidenced by a higher creatinine clearance (+348%) and lower levels o f blood urea nitrogen (-69%) and histological renal damage (-50%) comp ared with ischemic control animals. Indexes of kidney function in AZ-t reated animals subjected to RAO were not significantly different from those of nonischemic control animals. Two other nitrovasodilators, sod ium nitroprusside and hydralazine, at doses which produced decreases i n blood pressure similar to that of AZ, were ineffective at preventing ARF. The beneficial effect of AZ may be due to its known ability to i nhibit one or more enzymes including adenosinetriphosphatase, cytochro me-c oxidase, and myeloperoxidase.