Oxygen Sensing by Human Recombinant Large Conductance,Calcium-activated Potassium Channels
Although O2-sensitive tissues express a wide variety of channel types (Lopez-Barneo et al. 2001; Peers & Kemp, 2001), central to the cellular mechanism of O2 sensing in many is hypoxic suppression of large conductance Ca2+-activated K+ channels (maxiK, BKCa or Slo channels). Thus, hypoxic inhibition of maxiK channels has been demonstrated in carotid body (Peers, 1990; Pardal et al. 2000; Riesco-Fagundo et al. 2001), pulmonary smooth muscle (Cornfield et al. 1996), chromaffin cells (Thompson & Nurse, 1998), and other non-chemosensory tissues such as central neurones (Liu et al. 1999; Jiang & Haddad, 1994b). Contribution of this channel type to carotid body, chromatin cell and central neuronal function is well supported although some controversy still surrounds their involvement in pulmonary vasoconstriction (Ward & Aaronson, 1999) where there is also good evidence for both delayed rectifier (Tristani-Firouzi et al. 1996) and tandem P domain K+ channels in the response (Gurney et al. 2002); the later observation is fully supported by our recent report of O2 sensitivity of the tandem P domain channel, hTASKl, in a recombinant mammalian system similar to that employed in the present study (Lewis et al., 2001).
KeywordsCarotid Body Acute Hypoxia Pulmonary Artery Smooth Muscle Cell Asymmetrical Solution Cytosolic Factor
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- Jiang, C. & Haddad, G. G., 1994b, Oxygen deprivation inhibits a K+ channel independently of cytosolic factors in rat central neurons. J.Physiol. 481, 15–26.Google Scholar