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Extracellular pH alkalinization by Cl^–/HCO₃^– exchanger is crucial for TASK2 activation by hypotonic shock in proximal cell lines from mouse kidney

¹UMR Centre National de la Recherche Scientifique 6548, Université de Nice-Sophia Antipolis, Nice, and ²Institut de Pharmacologie du Centre National de la Recherche Scientifique, Valbonne Sophia-Antipolis, France

Submitted 18 April 2006 ; accepted in final form 20 September 2006

We have previously shown that K⁺-selective TASK2 channels and swelling-activated Cl^– currents are involved in a regulatory volume decrease (RVD; Barriere H, Belfodil R, Rubera I, Tauc M, Lesage F, Poujeol C, Guy N, Barhanin J, Poujeol P. J Gen Physiol 122: 177–190, 2003; Belfodil R, Barriere H, Rubera I, Tauc M, Poujeol C, Bidet M, Poujeol P. Am J Physiol Renal Physiol 284: F812–F828, 2003). The aim of this study was to determine the mechanism responsible for the activation of TASK2 channels during RVD in proximal cell lines from mouse kidney. For this purpose, the patch-clamp whole-cell technique was used to test the effect of pH and the buffering capacity of external bath on Cl^– and K⁺ currents during hypotonic shock. In the presence of a high buffer concentration (30 mM HEPES), the cells did not undergo RVD and did not develop outward K⁺ currents (TASK2). Interestingly, the hypotonic shock reduced the cytosolic pH (pH_i) and increased the external pH (pH_e) in wild-type but not in cftr ^–/– cells. The inhibitory effect of DIDS suggests that the acidification of pH_i and the alkalinization of pH_e induced by hypotonicity in wild-type cells could be due to an exit of HCO₃^–. In conclusion, these results indicate that Cl^– influx will be the driving force for HCO₃^– exit through the activation of the Cl^–/HCO₃^– exchanger. This efflux of HCO₃^– then alkalinizes pH_e, which in turn activates TASK2 channels.

regulatory volume decrease; CFTR; KCNE5; potassium and chloride channels; external and internal pH