Na⁺ dependence of K⁺‐induced natriuresis, kaliuresis and Na⁺/Cl⁻ cotransporter dephosphorylation

Abstract

These data indicate that acute K(+) -induced kaliuresis is ENaC dependent. Maximal K(+) excretion rates are attenuated when ENaC is physiologically down-regulated or pharmacologically blocked. NCC is dephosphorylated following acute K(+) loading under all dietary Na(+) regimens. This leads to natriuresis, even in severely Na(+) -restricted animals.