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Chemoreception pp 225-230 | Cite as

Sensory Neurons of Rat and Mice Dorsal Root Ganglia Respond to Hypoxia with Increased NO Generation

  • Michael Henrich
  • Peter König
  • Marco Gruß
  • Tamara Fischbach
  • Axel Gödecke
  • Gunter Hempelmann
  • Wolfgang Kummer
Conference paper
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 536)

Abstract

Studies on Drosophila larvae have added nitric oxide (NO) as another endogenous intracellular signalling molecule mediating hypoxia-induced adaptations (Wingrove and O'Farrell, 1999; DiGregorio et al. 2001). In mammalian cells, exogenously applied NO is able to interfere with the signalling cascades that are activated by low oxygen tension. NO treatment under normoxic conditions stabilizes hypoxia-inducible factor-la (HIF-la), the major transcription factor involved in hypoxia-regulated gene expression, and promotes its DNA-binding activity and downstream gene expression (Genius and Fandrey, 2000; Kimura et al. 2000; Palmer et al., 2000; Sandau et al. 2001). It is currently unclear, whether this effect is due to an interaction of NO with the iron containing HIF-modulating enzyme, HIF- prolyl-hydroxylase (Ivan et al. 2001; Jaakkola et al. 2001) or whether NO acts via a different pathway. Under hypoxic conditions, however, partly opposing effects of exogenously applied NO have been reported (Liu et al. 1998; Huang et al. 1999; Sogawa et al. 1998). One possible explanation is that NO may react with ROS formed during hypoxia to yield compounds such as peroxynitrite that do not stimulate HIF-la (Semenza, 2001). Similarly, the effect of NO on the skeletal muscle calcium release channel is critically dependent on pO2 (Eu et al. 2000). None of these studies reported on the endogenous production of NO under these conditions.

Keywords

Nitric Oxide Dorsal Root Ganglion Sensory Neuron Vascular Endothelial Growth Factor Gene Downstream Gene Expression 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 2003

Authors and Affiliations

  • Michael Henrich
    • 1
    • 2
  • Peter König
    • 2
  • Marco Gruß
    • 1
    • 3
  • Tamara Fischbach
    • 2
  • Axel Gödecke
    • 4
  • Gunter Hempelmann
    • 1
  • Wolfgang Kummer
    • 2
  1. 1.Department of Anaesthesiology, Intensive Care and Pain TherapyJustus-Liebig-UniversityGiessenGermany
  2. 2.Institute for Anatomy and Cell BiologyJustus-Liebig-UniversityGiessenGermany
  3. 3.Institute for PhysiologyJustus-Liebig-UniversityGiessenGermany
  4. 4.Institute for PhysiologyHeinrich-Heine UniversityDusseldorf Germany

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