Nitric oxide metabolism following unilateral renal ischemia/reperfusion injury in rats
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Experimental study Original article
Nitric oxide metabolism following unilateral renal ischemia/reperfusion injury in rats Wayne R. Waz, Judith B. Van Liew, and Leonard G. Feld Departments of Physiology and Pediatrics, State University of New York at Buffalo, The Children's Hospital of Buffalo, and Veterans Administration Medical Center, Buffalo, New York 14222, USA Received December 30, 1996; received in revised form July 17, 1997; accepted July 22, 1997
Abstract. Renal ischemia/reperfusion (I/R) injury results in decreased glomerular filtration and renal blood flow (RBF) and increased urine output, characterized by natriuresis and impaired concentrating ability. We studied unilateral I/R in rats to assess renal handling of nitric oxide (NO). Prior to I/ R, we measured urine flow rate (V), inulin clearance (CIN), para-aminohippuric acid clearance (CPAH), NO clearance (CNOx determined from metabolites NO2 and NO3), tubular transport of NOx (TNOx, filtered load + urinary excretion), urine sodium and potassium excretion (UNaV, UKV), fractional excretion of sodium (FENa), and fractional excretion of NOx (FENOx) in each kidney. The left renal artery was then ligated for 30 min, followed by 30 min of reperfusion, and all measurements were repeated. CIN and CPAH were decreased in I/R kidneys compared with the contralateral kidney or pre-ischemia controls. V, FENa, and UKV were all significantly increased in I/R kidneys. Plasma NOx concentration was lower after injury in all animals (23.3+2.8 post injury vs. 30.4+7.7 mM pre injury, P 50.05). CNOx was significantly higher in I/R kidneys (0.14+0.05 ml/min per g kidney weight) than in pre-injury kidneys (0.03+0.02 right, 0.04+0.30 left) or the contralateral controls (0.04+0.02) (P 50.05 for all three controls). TNOx showed net tubular reabsorption of NOx in all kidneys (11+6 in post-ischemic left kidneys vs. 25+20 in left pre-ischemia, 33+13 in right pre-ischemia, and 21+4 right post-ischemia, nM/min per g kidney weight, P = NS). FENOx was higher in injured kidneys (28%+18) than in pre-injury (3%+0.6, 5%+3) or contralateral controls (6%+3) (P 50.05 for all three controls). Renal NOx excretion and clearance are increased despite decreased plasma levels of NO metabolites after I/R injury. This increased excretion is not dependent on RBF or glomerular filtration, but may be related to impaired tubular reabsorption of NOx combined with increased intra-renal NO production. Correspondence to: W. R. Waz, Division of Nephrology, The Children's Hospital of Buffalo, 219 Bryant Street, Buffalo, NY 14 222, USA
Key words: Acute renal failure ± Renal clearance ± Tubular transport ± Sodium ± Potassium
Introduction In the kidney, the endothelium-derived relaxing factor nitric oxide (NO) influences many aspects of function, including autoregulation of blood flow, renin secretion, glomerular mesangial and epithelial cell activity, tubuloglomerular feedback, and tubular function [1, 2]. Basal production of NO is necessary for normal glomerular function, and NO synthesis inhibition leads to i
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