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Am J Physiol Renal Physiol (December 10, 2002). doi:10.1152/ajprenal.00237.2002
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Articles in PresS, published online ahead of print December 10, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00237.2002
Submitted on June 26, 2002
Accepted on December 3, 2002

CFTR NULL MUTATION ALTERED BOTH cAMP-SENSITIVE AND SWELLING-ACTIVATED Cl- CURRENTS IN PRIMARY CULTURES OF MOUSE NEPHRON

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

1 UMR6548, 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 Cl- currents was studied in mouse kidney. Using whole cell clamp Cl- currents were analyzed in primary cultures of proximal, distal convoluted (DCT) and cortical collecting tubule (CCT) from wild type (WT) and cftr knock-out (KO) mice. In WT mice, forskolin activated a linear Cl- current only in DCT and CCT cells. This current was not recorded in KO mice. In both mice, Ca2+-dependent Cl- currents were recorded in all segments. In WT mice, volume-sensitive Cl- currents were implicated in RVD during hypotonicity. In KO, RVD and swelling Cl- current were impaired but were restored by adenosine perfusion. Extracellular ATP also restored swelling Cl- currents. The effect of ATP or adenosine was blocked by DPCPX. The ecto-ATPase inhibitor (ARL67156) inhibited the effect of hypotonicity and ATP. Finally, in KO mice volume-sensitive Cl- currents are potentially functional but the absence of CFTR precludes their activation by extracellular nucleosides. This observation strengthens the hypothesis that CFTR is a modulator of ATP release in epithelia.




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