Reactive
oxygen and
nitrogen species play a key role in the pathophysiology of renal
ischemia-reperfusion (I/R) injury. Recent studies have shown that
nitrite (NO(2)(-)) serves as an endogenous source of
nitric oxide (NO), particularly in the presence of
hypoxia and
acidosis. Nanomolar concentrations of NO(2)(-) reduce injury following I/R in the liver and heart in vivo. The purpose of this study was to evaluate the role of NO(2)(-) in renal I/R injury. Male Sprague-Dawley rats underwent a unilateral
nephrectomy followed by 45 min of
ischemia of the contralateral kidney or
sham surgery under
isoflurane anesthesia. Animals received
normal saline,
sodium NO(2)(-), or
sodium nitrate (NO(3)(-); 1.2 nmol/g body wt ip) at 22.5 min after induction of
ischemia or 15 min before
ischemia. A separate set of animals received saline, NO(2)(-), or NO(3)(-) (0.12, 1.2, or 12 nmol/g body wt iv) 45 min before
ischemia. Serum
creatinine and blood
urea nitrogen were increased following I/R injury but were not significantly different among treatment groups at 24 and 48 h after
acute renal injury. Interestingly, NO(3)(-) administration appeared to worsen renal injury. Histological scoring for loss of brush border, tubular
necrosis, and red blood cell extravasation showed no significant differences among the treatment groups. The results indicate that, contrary to the protective effects of NO(2)(-) in I/R injury of the liver and heart, NO(2)(-) does not provide protection in renal I/R injury and suggest a unique metabolism of NO(2)(-) in the kidney.