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Significance Loss of function mutations in the potassium channel KCNJ10 causes a salt-wasting syndrome. The phenotype resembles Gitelman syndrome, which results from loss of sodium chloride transport along the distal convoluted tubule (DCT), but the mechanisms involved are not clear. Here, we perform experiments in the kidney from Kcnj10 knockout mice and demonstrate that Kcnj10 is a main contributor to the basolateral potassium conductance in the DCT and that the potassium channel activity regulates the expression of ste20-related proline–alanine-rich kinase (SPAK) and determines Na-Cl cotransporter (NCC) expression. Our study suggests the possibility that the regulation of basolateral Kcnj10 activity in the DCT may be the first step in response to a variety of physiological stimuli for initiating SPAK-WNK-dependent modulation of NCC expression in the kidney.

KCNJ10 determines the expression of the apical Na-Cl cotransporter (NCC) in the early distal convoluted tubule (DCT1)