Abstract
A low-Na(+), high-K(+) diet (LNaHK) is considered a healthier alternative to the "Western" high-Na(+) diet. Because the mechanism for K(+) secretion involves Na(+) reabsorptive exchange for secreted K(+) in the distal nephron, it is not understood how K(+) is eliminated with such low Na(+) intake. Animals on a LNaHK diet produce an alkaline load, high urinary flows, and markedly elevated plasma ANG II and aldosterone levels to maintain their K(+) balance. Recent studies have revealed a potential mechanism involving the actions of alkalosis, urinary flow, elevated ANG II, and aldosterone on two types of K(+) channels, renal outer medullary K(+) and large-conductance K(+) channels, located in principal and intercalated cells. Here, we review these recent advances.