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Nitric oxide synthase reduces nitrite to NO under anoxia
Authors:A F Vanin  L M Bevers  A Slama-Schwok  E E van Faassen
Institution:(1) Faculty of Science, Department of Interface Physics, Utrecht University, 3508, TA, Utrecht, The Netherlands;(2) Semenov Institute of Chemical Physics, Russian Academy of Sciences, Moscow, Russia;(3) Department of Nephrology and Hypertension, University Medical Center, Utrecht, The Netherlands;(4) Laboratory for Optics and Biosciences, Ecole Polytechnique, Palaiseau, France
Abstract:Cultured bEND.3 endothelial cells show a marked increase in NO production when subjected to anoxia, even though the normal arginine pathway of NO formation is blocked due to absence of oxygen. The rate of anoxic NO production exceeds basal unstimulated NO synthesis in normoxic cells. The anoxic release of NO is mediated by endothelial nitric oxide synthase (eNOS), can be abolished by inhibitors of NOS and is accompanied by consumption of intracellular nitrite. The anoxic NO release is unaffected by the xanthine oxidase inhibitor oxypurinol. The phenomenon is attributed to anoxic reduction of intracellular nitrite by eNOS, and its magnitude and duration suggests that the nitrite reductase activity of eNOS is relevant for fast NO delivery in hypoxic vascular tissues. Received 20 August 2006; received after revision 21 September 2006; accepted 8 November 2006
Keywords:Nitric oxide  nitrite  nitrite reductase  endothelial NOS  anoxia  ischemia
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