AJP - Renal Physiology, Vol 265, Issue 1 130-F136, Copyright © 1993 by American Physiological Society
Sodium azide protects against ischemia-induced acute renal failure in rats
S. L. Abrahams, R. J. Hazen and K. M. Ayers
Division of Pharmacology, Burroughs Wellcome, Research Triangle Park, North Carolina 27709.
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.
