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Potassium (K + ) intake is intrinsically linked to blood pressure. High-K + intake decreases hypertension and associated lower mortality. On the other hand, hyperkalemia causes sudden death with fatal cardiac arrhythmia and is also related to higher mortality. Renal sodium (Na + )-chloride (Cl ‒ ) cotransporter (NCC), expressed in the distal convoluted tubule, is a key molecule in regulating urinary K + excretion. K + intake affects the activity of the NCC, which is related to salt-sensitive hypertension. A K + -restrictive diet activates NCC, and K + loading suppresses NCC. Hyperpolarization caused by decreased extracellular K + concentration ([K + ] ex ) increases K + and Cl ‒ efflux, leading to the activation of Cl ‒ -sensitive with-no-lysine (WNK) kinases and their downstream molecules, including STE20/SPS1-related proline/alanine-rich kinase (SPAK) and NCC.

Clinical importance of potassium intake and molecular mechanism of potassium regulation