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00925njm 22002777a 4500 dc Dinger, Bruce author He, Le author Chen, J. author Liu, X. author González Martínez, Constancio author Sanders, K. author Hoidal, J. author Stensaas, L. author Fidone, Salvatore author Obeso Cáceres, Ana María de la Luz author 2007 O2-sensing in the carotid body occurs in neuroectoderm-derived type I glomus cells where hypoxia elicits a complex chemotransduction cascade involving membrane depolarization, Ca2+ entry and the release of excitatory neurotransmitters. Efforts to understand the exquisite O2-sensitivity of these cells currently focus on the coupling between local PO2 and the open-closed state of K+-channels. Amongst multiple competing hypotheses is the notion that K+-channel activity is mediated by a phagocytic-like multisubunit enzyme, NADPH oxidase, which produces reactive oxygen species (ROS) in proportion to the prevailing PO2. In O2-sensitive cells of lung neuroepithelial bodies (NEB), multiple studies confirm that ROS levels decrease in hypoxia, and that EM and K+-channel activity are indeed controlled by ROS produced by NADPH oxidase. However, recent studies in our laboratories suggest that ROS generated by a non-phagocyte isoform of the oxidase are important contributors to chemotransduction, but that their role in type I cells differs fundamentally from the mechanism utilized by NEB chemoreceptors. Data indicate that in response to hypoxia, NADPH oxidase activity is increased in type I cells, and further, that increased ROS levels generated in response to low-O2 facilitate cell repolarization via specific subsets of K+-channels. Respiratory Physiology & Neurobiology 157 (2007) 45–54 1569-9048 http://uvadoc.uva.es/handle/10324/7156 10.1016/j.resp.2006.12.003 45 54 Respiratory Physiology & Neurobiology 157 Neurofisiologia The role of NADPH oxidase in carotid body arterial chemoreceptors