RT info:eu-repo/semantics/article
T1 The role of NADPH oxidase in carotid body arterial chemoreceptors
A1 Dinger, Bruce
A1 He, Le
A1 Chen, J.
A1 Liu, X.
A1 González, Constancio
A1 Obeso Cáceres, Ana María de la Luz
A1 Sanders, K.
A1 Hoidal, J.
A1 Stensaas, L.
A1 Fidone, Salvatore
K1 Neurofisiologia
AB O2-sensing in the carotid body occurs in neuroectoderm-derived type I glomus cells where hypoxia elicits a complex chemotransduction cascadeinvolving membrane depolarization, Ca2+ entry and the release of excitatory neurotransmitters. Efforts to understand the exquisite O2-sensitivity ofthese cells currently focus on the coupling between local PO2 and the open-closed state of K+-channels. Amongst multiple competing hypothesesis the notion that K+-channel activity is mediated by a phagocytic-like multisubunit enzyme, NADPH oxidase, which produces reactive oxygenspecies (ROS) in proportion to the prevailing PO2. In O2-sensitive cells of lung neuroepithelial bodies (NEB), multiple studies confirm that ROSlevels decrease in hypoxia, and that EM and K+-channel activity are indeed controlled by ROS produced by NADPH oxidase. However, recentstudies 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 tohypoxia, NADPH oxidase activity is increased in type I cells, and further, that increased ROS levels generated in response to low-O2 facilitate cellrepolarization via specific subsets of K+-channels.
PB Elsevier
SN 1569-9048
YR 2007
FD 2007
LK http://uvadoc.uva.es/handle/10324/7156
UL http://uvadoc.uva.es/handle/10324/7156
LA eng
NO Respiratory Physiology & Neurobiology 157 (2007) 45–54
NO Producción Científica
DS UVaDOC
RD 18-abr-2024