Sustained Hypoxia Enhances TASK-like Current Inhibition by Acute Hypoxia in Rat Carotid Body Type-I Cells
Carotid body type-I cells respond to acute hypoxia with membrane depolarization and calcium-dependentneurotransmitter release. The inhibition of a TASK-like background potassium channels plays a key role in initiating this response. Chronic hypoxia enhances the carotid body chemosensory responses evoked by acute hypoxia, however the accurate mechanism by which chronic hypoxia increases carotid body reactivity is not clear. Therefore, we investigated the effects of chronic hypoxia upon TASK-like currents in isolated type-I cells. Carotid bodies were excised from anaesthetized newborn Sprague-Dawley rats and dissociated by collagenase-trypsin digestion. Isolated cells were maintained under 5% CO 2 in normoxic (21% O 2) or hypoxic (1-2% O 2) environment for 24 and 48 hours. Channel activity (NPo) was recorded using the cell-attached configuration of the patch-clamp technique. In normoxic and 24 hours hypoxic cultured cells, acute hypoxic stimuli decreases NPo approximately 70% with no effects on current amplitude. On the other hand, in cultured cells subjected to 48 hours of hypoxia, NPo decreases near to 90% in response to acute hypoxia. We concluded that continuous hypoxic exposure enhances the TASK-like channel activity inhibition in response to acute hypoxia. Our results provide a potential mechanism by which chronic hypoxia increases carotid body reactivity. © Springer Science+Business Media B.V. 2009.
|Título según WOS:||Sustained Hypoxia Enhances TASK-like Current Inhibition by Acute Hypoxia in Rat Carotid Body Type-I Cells|
|Título según SCOPUS:||Sustained hypoxia enhances TASK-like current inhibition by acute hypoxia in rat carotid body type-I cells|
|Título de la Revista:||Advances in Experimental Medicine and Biology|
|Editorial:||Springer New York LLC|
|Fecha de publicación:||2009|
|Página de inicio:||83|