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Low pO2 selectively inhibits K channel activity in chemoreceptor cells of the mammalian carotid body


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dc.creator López López, J.
dc.creator González Montelongo, M. Carmen
dc.creator Ureña López, Juan
dc.creator López Barneo, José 2015-01-16T13:21:11Z 2015-01-16T13:21:11Z 1989
dc.identifier.issn 1540-7748 es
dc.identifier.issn 0022-1295 es
dc.description.abstract The hypothesis that changes in environmental O2 tension (pO2) could affect the ionic conductances of dissociated type I cells of the carotid body was tested. Cells were subjected to whole-cell patch clamp and ionic currents were recorded in a control solution with normal pO2 (pO2 = 150 mmHg) and 3-5 min after exposure to the same solution with a lower pO2. Na and Ca currents were unaffected by lowering pO2 to 10 mmHg, however, in all cells studied (n = 42) exposure to hypoxia produced a reversible reduction of the K current. In 14 cells exposed to a pO2 of 10 mmHg peak K current amplitude decreased to 35 +/- 8% of the control value. The effect of low pO2 was independent of the internal Ca2+ concentration and was observed in the absence of internal exogenous nucleotides. Inhibition of K channel activity by hypoxia is a graded phenomenon and in the range between 70 and 120 mmHg, which includes normal pO2 values in arterial blood, it is directly correlated with pO2 levels. Low pO2 appeared to slow down the activation time course of the K current but deactivation kinetics seemed to be unaltered. Type I cells subjected to current clamp generate large Na- and Ca-dependent action potentials repetitively. Exposure to low pO2 produces a 4-10 mV increase in the action potential amplitude and a faster depolarization rate of pacemaker potentials, which leads to an increase in the firing frequency. Repolarization rate of individual action potentials is, however, unaffected, or slightly increased. The selective inhibition of K channel activity by low pO2 is a phenomenon without precedents in the literature that explains the chemoreceptive properties of type I cells. The nature of the interaction of molecular O2 with the K channel protein is unknown, however, it is argued that a hemoglobin-like O2 sensor, perhaps coupled to a G protein, could be involved. es
dc.language.iso eng es
dc.relation.ispartof The Journal of general physiology, 93 (5), 1001-1015. es
dc.rights Atribución-NoComercial-SinDerivadas 4.0 España *
dc.rights.uri *
dc.title Low pO2 selectively inhibits K channel activity in chemoreceptor cells of the mammalian carotid body
dc.type info:eu-repo/semantics/article es
dc.rights.accessrights info:eu-repo/semantics/openAccess es
dc.contributor.affiliation Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica es
dc.journaltitle The Journal of general physiology es
dc.publication.volumen 93 es
dc.publication.issue 5 es
dc.publication.initialPage 1001 es
dc.publication.endPage 1015 es
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