Exchangers and Cotransporters

A decrease below the threshold Pq, normally close to 50 Torr, in glomus cells of the carotid body or in the neonatal ductus arteriosus results in an inhibition of the tonic K current. Such oxygen-regulated inhibition of K+ channels, which may be mediated by mitochondria-derived hydrogen peroxide (Archer et al., 2004), results in an increase in cellular excitability, increased Ca + influx, and a resultant increase in the level of Ca + in the cytosol (reviewed by Lopez-Barneo et al., 1999). 

Neuroepithelial bodies found in mammalian airways have oxygen-sensitive K currents and are putative airway chemoreceptors that detect changes in the level of O2 in the airway lumen (Wang et al., 

Exposure to acute hypoxia in vivo (Lauweryns et al., 1987) or in vitro (Fu et al., 2002) results in serotonin release, which may have a role in controlling pulmonary vascular tone. The oxygen sensitivity of these channels may result from their close localization to membrane-bound cytochromes (Youngson et al., 

It is clear that the closure of voltage-gated K charmels by hypoxic exposure has implications for neuroprotection as demonstrated by K+ channel arrest in hypoxia-tolerant turtles (Pek and Lutz, 1997 Bidder and Buck, 1998 Hochachka and Lutz, 2001 Bidder and Donohoe, 2002), which reduces Ca influx (Bidder and Buck, 1998). In some anoxia-tolerant spedes, neuronal energy is not only conserved by ion channel arrest but also by ATP-sensitive mitochondrial K+ channel arrest (reviewed by Buck and Pamenter, 2006). This may have implications for chnical interventions. 

Oxygen sensors of the peripheral and central nervous systems 

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