2026-04-14T19:41:05Zhttps://uvadoc.uva.es/oai/request

oai:uvadoc.uva.es:10324/71562025-03-03T10:32:21Zcom_10324_1134com_10324_931com_10324_894col_10324_1213

Dinger, Bruce He, Le Chen, J. Liu, X. González Martínez, Constancio Sanders, K. Hoidal, J. Stensaas, L. Fidone, Salvatore Obeso Cáceres, Ana María de la Luz 2014-11-14T12:01:12Z 2014-11-14T12:01:12Z 2007 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 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. eng info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by-nc-nd/4.0/ Attribution-NonCommercial-NoDerivatives 4.0 International Neurofisiologia The role of NADPH oxidase in carotid body arterial chemoreceptors info:eu-repo/semantics/article