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Oxygen-sensing by ion channels and mitochondrial function in carotid body glomus cells
dc.creator | López Barneo, José | |
dc.creator | Ortega Sáenz, Patricia | |
dc.creator | Piruat Palomo, José Ignacio | |
dc.creator | García Fernández, María | |
dc.date.accessioned | 2015-01-22T11:39:10Z | |
dc.date.available | 2015-01-22T11:39:10Z | |
dc.date.issued | 2006 | |
dc.identifier.citation | López Barneo, J., Ortega Sáenz, P., Piruat Palomo, J.I. y García Fernández, M. (2006). Oxygen-sensing by ion channels and mitochondrial function in carotid body glomus cells. En Novartis Foundation Symposium John Wiley & Sons. | |
dc.identifier.isbn | 9780470034996 | es |
dc.identifier.uri | http://hdl.handle.net/11441/18238 | |
dc.description.abstract | Carotid body glomus cells release transmitters in response to hypoxia due to the increase of excitability resulting from inhibition of O2-regulated K+ channels. The mechanisms involved in the detection of changes of O2 tension are unknown. Inhibition of the mitochondrial electron transport chain (ETC) at proximal and distal complexes induces external Ca2+-dependent catecholamine secretion. At saturating concentration of the ETC inhibitors, the cellular response to hypoxia is maintained. However, rotenone, a complex I blocker, selectively occludes the responsiveness to hypoxia of glomus cells in a dosedependent manner. The effect of rotenone is not mimicked by complex I inhibitors acting on different sites. We have also generated a knock-out mouse lacking SDHD, the small membrane-anchoring protein of the succinate dehydrogenase (complex II) of the mitochondrial electron transport chain. Homozygous Sdhd -/- animals die at early embryonic stages. Heterozygous Sdhd +/- mice show a general, non-compensated, deficiency of complex II activity, and abnormal enhancement of resting carotid body secretion rate due to decrease of K+ conductance and persistent Ca2+ influx into glomus cells. However, responsiveness to hypoxia of carotid bodies from Sdhd +/- mice remains intact. These data strongly suggest that sensitivity to hypoxia of carotid body glomus cells is not linked in a simple way to mitochondrial electron flow. Nevertheless, it is possible that a rotenone-sensitive molecule critically participates in acute carotid body oxygen sensing. | es |
dc.language.iso | eng | es |
dc.publisher | John Wiley & Sons | es |
dc.relation.ispartof | Novartis Foundation Symposium (2006), | |
dc.rights | Atribución-NoComercial-SinDerivadas 4.0 España | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.title | Oxygen-sensing by ion channels and mitochondrial function in carotid body glomus cells | |
dc.type | info:eu-repo/semantics/conferenceObject | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica | es |
dc.eventtitle | Novartis Foundation Symposium | |
dc.identifier.idus | https://idus.us.es/xmlui/handle/11441/18238 |
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