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Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Respir+Physiol+Neurobiol 2011 ; 177 (3): 247-55 Nephropedia Template TP
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Characterization of an ATP-sensitive K(+) channel in rat carotid body glomus cells #MMPMID21536154
Kim D; Kim I; Papreck JR; Donnelly DF; Carroll JL
Respir Physiol Neurobiol 2011[Aug]; 177 (3): 247-55 PMID21536154show ga
Carotid body glomus (CB) cells express different types of K(+) channels such as TASK, BK, and Kv channels, and hypoxia has been shown to inhibit these channels. Here we report the presence of a approximately 72-pS channel that has not been described previously in CB cells. In cell-attached patches with 150 mM K(+) in the pipette and bath solutions, TASK-like channels were present ( approximately 15 and approximately 36-pS). After formation of inside-out patches, a 72-pS channel became transiently active in approximately 18% of patches. The 72-pS channel was K(+)-selective, inhibited by 2-4 mM ATP and 10-100 muM glybenclamide. The 72-pS channel was observed in CB cells isolated from newborn, 2-3 week and 10-12 week-old rats. Reverse transcriptase-PCR and immunocytochemistry showed that Kir6.1, Kir6.2, SUR1 and SUR2 were expressed in CB glomus cells as well as in non-glomus cells. Acute hypoxia ( approximately 15 mmHg O(2)) inhibited TASK-like channels but failed to activate the 72-pS channel in cell-attached CB cells. K(+) channel openers (diazoxide, pinacidil, levcromakalim), sodium cyanide and removal of extracellular glucose also did not activate the 72-pS channel in the cell-attached state. The hypoxia-induced elevation of intracellular [Ca(2+)] was unchanged by glybenclamide or diazoxide. NaCN-induced increase in [Ca(2+)] was not affected by 10 muM glybenclamide but inhibited by 100 muM glybenclamide. Acute glucose deprivation did not elevate [Ca(2+)] in the presence or absence of glybenclamide. These results show that an ATP-sensitive K(+) channel is expressed in the plasma membrane of CB cells, but is not activated by short-term metabolic inhibition. The functional relevance of the 72-pS channel remains to be determined.