Cellular and Molecular Life Sciences

, Volume 64, Issue 1, pp 96–103

Nitric oxide synthase reduces nitrite to NO under anoxia

Authors

  • A. F. Vanin
    • Faculty of Science, Department of Interface PhysicsUtrecht University
    • Semenov Institute of Chemical PhysicsRussian Academy of Sciences
  • L. M. Bevers
    • Department of Nephrology and HypertensionUniversity Medical Center
  • A. Slama-Schwok
    • Laboratory for Optics and BiosciencesEcole Polytechnique
    • Faculty of Science, Department of Interface PhysicsUtrecht University
    • Semenov Institute of Chemical PhysicsRussian Academy of Sciences
Research Article

DOI: 10.1007/s00018-006-6374-2

Cite this article as:
Vanin, A.F., Bevers, L.M., Slama-Schwok, A. et al. Cell. Mol. Life Sci. (2007) 64: 96. doi:10.1007/s00018-006-6374-2

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.

Keywords.

Nitric oxide nitrite nitrite reductase endothelial NOS anoxia ischemia

Copyright information

© Birkhäuser Verlag, Basel 2007