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Received March 1, 2005
Revised April 7, 2005
Accepted after revision May 5, 2005
1 Ludwig Maximilians Universität München
2 Universidad de Valladolid
* To whom correspondence should be addressed. E-mail: tperez{at}ibgm.uva.es.
The carotid body (CB) chemoreceptors participate in the ventilatory responses to acute and chronic hypoxia (CH). Arterial hypoxemia increases breathing within seconds, and CB chemoreceptors are the principal contributors to this reflex hyperventilatory response. Acute hypoxia induces depolarisation of CB chemoreceptors by inhibiting certain K+ channels, but the role of these channels in CH, as in high altitude acclimatization, is less known. Here we explored the effects of prolonged (24-48h) hypoxic exposure of rabbit CB chemoreceptor cells in primary cultures on the voltage-dependent K+ currents and on their response to acute hypoxia. We found that CH induces a decrease in the amplitude of outward K+ currents due to a reduction in a fast-inactivating, BDS- and highly TEA-sensitive, component of the current. In spite of this effect, acute hypoxic inhibition of K+ currents is increased in CH cultures, as well as hypoxia-induced depolarisation. These data suggest that down-regulation of this component (that does not contribute to the O2-sensitive K+ current (KO2)) participates in the hypoxic sensitisation. Pharmacological, immunocytochemical and quantitative PCR (qPCR) experiments demonstrate that CH induced decrease in outward K+ currents is due to a down-regulation of the expression of Kv3.4 channels. Taken together, our results suggest that CH sensitisation in rabbit CB could be achieved by an increase in the relative contribution of KO2 to the outward K+ current as a consequence of the decreased expression of the O2-insensitive component of the current. We conclude that acute and chronic hypoxia can exert their effects acting on different molecular targets.
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