Lack of contribution of mitochondrial electron transport to acute O2 sensing in model airway chemoreceptors

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 O2 to k+ channel inhibition and report that, in complete contrast to recent suggestions in pulmonary vasculature, O2 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 O2 species is not the unifying mechanism in O2 sensing