The mammalian distal convoluted tubule (DCT) makes an important contribution to
potassium homeostasis by modulating NaCl transport. The thiazide-sensitive Na+/Cl−
cotransporter (NCC) is activated by low potassium intake and by hypokalemia. Coupled with
suppression of aldosterone secretion, activation of NCC helps to retain potassium by
increasing electroneutral NaCl reabsorption, therefore reducing Na+/K+ exchange. Yet the
mechanisms by which DCT cells sense plasma potassium concentration and transmit the …