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This Article Full Text Full Text (PDF) All Versions of this Article: 297/3/C715    most recent 00507.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Gomez-Niño, A. Articles by Gonzalez, C. PubMed PubMed Citation Articles by Gomez-Niño, A. Articles by Gonzalez, C.

MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

MaxiK potassium channels in the function of chemoreceptor cells of the rat carotid body

¹Departamento de Bioquímica y Biología Molecular y Fisiología, ²Departamento de Biología Celular y Farmacología, e ³Instituto de Biología y Genética Molecular, Universidad de Valladolid, Consejo Superior de Investigaciones Científicas; and ⁴El Centro de Investigación Biomédica en Red de Enfermedades Respiratorias, Instituto de Salud Carlos III; Facultad de Medicina, Universidad de Valladolid Valladolid, Spain

Submitted 8 October 2008 ; accepted in final form 23 June 2009

Hypoxia activates chemoreceptor cells of the carotid body (CB) promoting an increase in their normoxic release of neurotransmitters. Catecholamine (CA) release rate parallels the intensity of hypoxia. Coupling of hypoxia to CA release requires cell depolarization, produced by inhibition of O₂-regulated K⁺ channels, and Ca²⁺ entering the cells via voltage-operated channels. In rat chemoreceptor cells hypoxia inhibits large-conductance, calcium-sensitive K channels (maxiK) and a two-pore domain weakly inward rectifying K⁺ channel (TWIK)-like acid-sensitive K⁺ channel (TASK)-like channel, but the significance of maxiK is controversial. A proposal envisions maxiK contributing to set the membrane potential (E_m) and the hypoxic response, but the proposal is denied by authors finding that maxiK inhibition does not depolarize chemoreceptor cells or alters intracellular Ca²⁺ concentration or CA release in normoxia or hypoxia. We found that maxiK channel blockers (tetraethylammonium and iberiotoxin) did not modify CA release in rat chemoreceptor cells, in either normoxia or hypoxia, and iberiotoxin did not alter the Ca²⁺ transients elicited by hypoxia. On the contrary, both maxiK blockers increased the responses elicited by dinitrophenol, a stimulus we demonstrate does not affect maxiK channels in isolated patches of rat chemoreceptor cells. We conclude that in rat chemoreceptor cells maxiK channels do not contribute to the genesis of the E_m, and that their full inhibition by hypoxia, preclude further inhibition by maxiK channel blockers. We suggest that full inhibition of this channel is required to generate the spiking behavior of the cells in acute hypoxia.

hypoxia; catecholamine; iberiotoxin; intracellular calcium