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Am J Physiol Renal Physiol (December 10, 2002). doi:10.1152/ajprenal.00238.2002
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Articles in PresS, published online ahead of print December 10, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00238.2002
Submitted on June 26, 2002
Accepted on December 3, 2002

CFTR DEPENDENT AND INDEPENDENT SWELLING-ACTIVATED K+ CURRENTS IN PRIMARY CULTURES OF MOUSE NEPHRON

RADIA BELFODIL1, HERVE BARRIERE1, ISABELLE RUBERA1, MICHEL TAUC1, CHANTAL POUJEOL1, MICHEL BIDET1, and PHILIPPE POUJEOL1*

1 UMR 6548, CNRS, Universite de Nice-Sophia Antipolis, NICE CEDEX 2, France

* To whom correspondence should be addressed. E-mail: poujeol{at}unice.fr.

The role of CFTR in the control of K+ currents was studied in mouse kidney. Using whole cell clamp, K+ currents were identified on the basis pharmacological sensitivities in primary cultures of proximal, distal convoluted (DCT) and cortical collecting tubule (CCT) from wild type (WT) and cftr knock-out (KO) mice. In DCT and CCT cells, forskolin activated a 293B-sensitive K+ current in WT but not in KO mice. In these cells, a hypotonic shock induced K+ currents blocked by charybdotoxin in WT but not in KO mice. In PCT cells from WT and KO mice, the hypotonicity-induced K+ currents were insensitive to these toxins and were activated at extracellular pH 8.0 and inhibited at pH 6.0 suggesting that the corresponding channel was TASK2. In conclusion CFTR is implicated in the control of KCNQ1 and Ca2+-sensitive swelling K+ conductances in DCT and CCT but not in PCT cells. In KO mice the impairment of RVD process in DCT and CCT could be due to the loss of an autocrine mechanism implicating ATP and adenosine which controls both swelling Cl- and K+ channels.




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