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lüll The role of NADPH oxidase in carotid body arterial chemoreceptors Dinger B; He L; Chen J; Liu X; Gonzalez C; Obeso A; Sanders K; Hoidal J; Stensaas L; Fidone SRespir Physiol Neurobiol 2007[Jul]; 157 (1): 45-54O(2)-sensing in the carotid body occurs in neuroectoderm-derived type I glomus cells where hypoxia elicits a complex chemotransduction cascade involving membrane depolarization, Ca(2+) entry and the release of excitatory neurotransmitters. Efforts to understand the exquisite O(2)-sensitivity of these cells currently focus on the coupling between local P(O2) 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 P(O2). In O(2)-sensitive cells of lung neuroepithelial bodies (NEB), multiple studies confirm that ROS levels decrease in hypoxia, and that E(M) 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-O(2) facilitate cell repolarization via specific subsets of K(+)-channels.|Animals[MESH]|Arteries/enzymology/innervation[MESH]|Carotid Body/*enzymology[MESH]|Chemoreceptor Cells/*enzymology[MESH]|Humans[MESH]|Mechanotransduction, Cellular/*physiology[MESH]|NADPH Oxidases/*metabolism[MESH]|Potassium Channels/metabolism[MESH]|Reactive Oxygen Species/metabolism[MESH] |