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1 Department of Medicine, Nephrology Research and Training Center, University of Alabama at Birmingham, Birmingham, Alabama, USA
2 Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USA
3 Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USA; Center for Free Radial Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA
4 Department of Medicine, Nephrology Research and Training Center, University of Alabama at Birmingham, Birmingham, Alabama, USA; Center for Free Radial Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA
* To whom correspondence should be addressed. E-mail: agarwal{at}uab.edu.
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 (NO2-) serves as an endogenous source of nitric oxide (NO) particularly in the presence of hypoxia and acidosis. Nanomolar concentrations of NO2- reduce injury following I-R in the liver and heart in vivo. The purpose of this study was to evaluate the role of NO2- in renal I-R injury. Male Sprague Dawley rats underwent unilateral nephrectomy followed by 45 min of ischemia of the contralateral kidney or sham surgery under isoflurane anesthesia. Animals received normal saline, sodium NO2- or sodium nitrate (NO3-) (1.2 nmol/gm body weight) by intraperitoneal administration at 22.5 min of induction of ischemia or 15 min prior to ischemia. A separate set of animals received saline, NO2- or NO3- (0.12, 1.2 or 12 nmol/gm body weight) intravenously 45 min prior to ischemia. Serum creatinine and 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, NO3- 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 NO2- in I-R injury of the liver and heart, NO2- does not provide protection in renal I-R injury and suggest a unique metabolism of NO2- in the kidney.
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