Dietary potassium deficiency, common in modern diets, raises blood pressure and enhances salt sensitivity. Potassium homeostasis requires a molecular switch in the distal convoluted tubule (DCT), which fails in familial hyperkalemic hypertension (pseudohypoaldosteronism type 2), activating the thiazide-sensitive NaCl cotransporter, NCC. Here, we show that dietary potassium deficiency activates NCC, even in the setting of high salt intake, thereby causing sodium retention and a rise in blood pressure. The effect is dependent on plasma potassium, which modulates DCT cell membrane voltage and, in turn, intracellular chloride. Low intracellular chloride stimulates WNK kinases to activate NCC, limiting potassium losses, even at the expense of increased blood pressure. These data show that DCT cells, like adrenal cells, sense potassium via membrane voltage. In the DCT, hyperpolarization activates NCC via WNK kinases, whereas in the adrenal gland, it inhibits aldosterone secretion. These effects work in concert to maintain potassium homeostasis. Display omitted •Dietary potassium deficiency activates thiazide-sensitive NaCl cotransport•Plasma potassium’s effects on NCC are mediated by membrane voltage•Membrane voltage alters cell chloride, affecting WNK kinase activity•Defects in distal potassium sensing cause human disease Terker et al. show that dietary potassium deficiency stimulates renal NaCl reabsorption, even in the setting of high salt intake, by hyperpolarizing distal convoluted tubule cells and reducing cell chloride. Low chloride activates WNK kinases, which stimulate the NaCl cotransporter, limiting potassium loss but raising arterial pressure.