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Am J Physiol Renal Physiol 284: F796-F811, 2003. First published December 10, 2002; doi:10.1152/ajprenal.00237.2002
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Vol. 284, Issue 4, F796-F811, April 2003

CFTR null mutation altered cAMP-sensitive and swelling-activated Clminus currents in primary cultures of mouse nephron

Hervé Barrière, Radia Belfodil, Isabelle Rubera, Michel Tauc, Chantal Poujeol, Michel Bidet, and Philippe Poujeol

Unité Mixte de Recherche Centre National de la Recherche Scientifique 6548, Université de Nice-Sophia Antipolis, 06108 Nice Cedex 2, France

The role of cystic fibrosis transmembrane conductance regulator (CFTR) in the control of Cl- currents was studied in mouse kidney. Whole cell clamp was used to analyze Cl- currents in primary cultures of proximal and distal convoluted and cortical collecting tubules from wild-type (WT) and cftr knockout (KO) mice. In WT mice, forskolin activated a linear Cl- current only in distal convoluted and cortical collecting tubule 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 regulatory volume decrease during hypotonicity. In KO mice, regulatory volume decrease and swelling-activated Cl- current were impaired but were restored by adenosine perfusion. Extracellular ATP also restored swelling-activated Cl- currents. The effect of ATP or adenosine was blocked by 8-cyclopentyl-1,3-diproxylxanthine. The ecto-ATPase inhibitor ARL-67156 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.

kidney; cystic fibrosis; cell volume; regulatory volume decrease


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