Clinical importance of potassium intake and molecular mechanism of potassium regulation

摘要

IntroductionPotassium (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.