Sodium azide protects against ischemia-induced acute renal failure in rats

Abstract

Sodium azide (AZ) is a nitrovasodilator with diverse biochemical properties. We found that low doses of AZ led to a profound protective effect against postischemic, acute renal failure (ARF) in rats. AZ, given at 250 micrograms/kg iv, before 25 min of renal artery occlusion (RAO) and again before reperfusion, conferred almost complete protection against loss of kidney function determined 18 h after RAO. The effect of AZ was evidenced by a higher creatinine clearance (+348%) and lower levels of blood urea nitrogen (-69%) and histological renal damage (-50%) compared with ischemic control animals. Indexes of kidney function in AZ-treated animals subjected to RAO were not significantly different from those of nonischemic control animals. Two other nitrovasodilators, sodium nitroprusside and hydralazine, at doses which produced decreases in 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 inhibit one or more enzymes including adenosinetriphosphatase, cytochrome-c oxidase, and myeloperoxidase.