title: Inhibition of nitric oxide synthase does not influence urinary nitrite plus nitrate excretion after renal ischemic injury.
abstract: OBJECTIVE
  Whether renal nitric oxide production caused by ischemia/reperfusion (I/R) influences the urinary excretion of nitric oxide (NO) metabolites (nitrite and nitrate) is far from being elucidated. In the present study, we evaluated the role of NO synthase inhibition using N(G)-nitro- L-arginine methyl ester ( L-NAME) in a model of experimental renal I/R injury.
  
  
  METHODS
  Male Wistar rats were used in our experiments, and renal I/R injury was achieved after a 30-min occlusion of the bilateral renal artery followed by a 60-min period of reperfusion. Renal function including nitrite plus nitrate excretion and hemodynamics in reperfused kidneys were measured in the presence and absence of L-NAME.
  
  
  RESULTS
  Intravenous application of L-NAME (5 mg/kg body weight) resulted in a marked reduction of urine flow, renal plasma flow (0.7 +/- 0.3 ml/min), and the glomerular filtration rate (0.1 +/- 0.01 ml/min), but a significant increase in NO excretion (FENOx, 67.9 +/- 10.5%). In addition we found after L-NAME injection a significant increase of the fractional excretion of sodium (FENa, 49.3 +/- 7.7%) and lithium (FELi, 70.2 +/- 1.6%), as well as the renal vascular resistance compared with animals with renal I/R but non-treated with L-NAME ( P<0.001). Furthermore, we observed a high correlation between FENOx and FELi (r(2)=0.80, P<0.01).
  
  
  CONCLUSIONS
  Our results suggest that renal excretion of NO derivatives is not influenced by NO production during renal I/R injury, although NO contributes to the tubular transport capacity in the ischemia/reperfused kidney.
authors.affiliation: Department of General Surgery, University of Ulm, Steinhövelstrasse 9, 89075 Ulm, Germany.
authors.forename: Toshihisa
authors.initials: T
authors.lastname: Ogawa
authors.forename: Andreas K
authors.initials: AK
authors.lastname: Nussler
authors.forename: Eda
authors.initials: E
authors.lastname: Tuzuner
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Mimura
authors.forename: Michio
authors.initials: M
authors.lastname: Kaminishi
authors.forename: Hans G
authors.initials: HG
authors.lastname: Beger
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D007511:Ischemia / Q000378:metabolism*; D007668:Kidney / Q000187:drug effects / Q000293:injuries* / Q000378:metabolism*; D007684:Kidney Tubules / Q000187:drug effects / Q000378:metabolism; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D009566:Nitrates / Q000652:urine*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors* / Q000494:pharmacology*; D009573:Nitrites / Q000652:urine*; D051381:Rats; D017208:Rats, Wistar; D012079:Renal Circulation / Q000187:drug effects / Q000502:physiology*; D015427:Reperfusion Injury / Q000378:metabolism*; D013997:Time Factors
chemical_list: D009566:Nitrates; D009573:Nitrites; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester