Among the several types of cells composing the airway epithelium, the ciliary cells are responsible for one of the most important defense mechanisms of the airway epithelium: the transport of inhaled particles back up into the throat by coordinated ciliary movement. Changes in the cytoplasmic Ca 21 concentration ([Ca 21 ] i ) are the main driving force controlling the ciliary activity. In mouse ciliary cells, membrane hyperpolarization from 220 to 260 mV under whole-cell voltage-clamp induced a slow but significant [Ca 21 ] i rise in a reversible manner. This rise was completely inhibited by the removal of Ca 21 from the extracellular solution. Application of diazoxide, an ATP-dependent K 1 channel opener, dose-dependently induced a membrane hyperpolarization (EC 50 5 2.3 mM), which was prevented by the addition of 5 mM glibenclamide. An inwardly rectifying current was elicited by the application of 10 mM diazoxide and suppressed by subsequent addition of 5 mM glibenclamide. Moreover, the application of 10 mM diazoxide induced a significant [Ca 21 ] i rise and facilitated ciliary movement. Multi-cell reverse-transcription polymerase chain reaction analyses and immunocytochemical staining suggested that the subunit combination of Kir6.2/SUR2B and possibly also Kir6
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