Lack of contribution of mitochondrial electron transport to acute O(2) sensing in model airway chemoreceptors

Biochem Biophys Res Commun. 2002 Feb 22;291(2):332-7. doi: 10.1006/bbrc.2002.6428.

Abstract

We have recently reported that the model airway chemoreceptors, H146 cells, exhibit a significant component of their oxygen-sensing transduction pathway which cannot be explained by activity of NADPH oxidase. Using patch-clamp, we have studied the transduction system linking reduced O(2) to k(+) channel inhibition and report that, in complete contrast to recent suggestions in pulmonary vasculature, O(2) sensing by the model airway chemoreceptors, H146 cells, does not require functional mitochondria. These data show, for the first time, that mitochondrial production of reactive O(2) species is not the unifying mechanism in O(2) sensing.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antimycin A / pharmacology
  • Cell Hypoxia
  • Chemoreceptor Cells / physiology*
  • DNA, Mitochondrial / genetics
  • Dose-Response Relationship, Drug
  • Electric Conductivity
  • Electron Transport / physiology
  • Humans
  • Kinetics
  • Methacrylates
  • Mitochondria / metabolism*
  • Mitochondria / physiology*
  • Patch-Clamp Techniques
  • Potassium Channel Blockers
  • Respiratory System / metabolism
  • Rotenone / pharmacology
  • Thiazoles / pharmacology
  • Tumor Cells, Cultured

Substances

  • DNA, Mitochondrial
  • Methacrylates
  • Potassium Channel Blockers
  • Thiazoles
  • Rotenone
  • Antimycin A
  • myxothiazol