Abstract
Renal K(+) excretion is increased rapidly following dietary K(+) intake, but the underlying molecular mechanisms are largely unknown. Sorensen and colleagues show that K(+) intake in mice provoked rapid and near-complete dephosphorylation of the renal distal convoluted tubule NaCl cotransporter, temporally associated with increases in both Na(+) and K(+) excretion. This response was independent of aldosterone and may be a crucial component of the acute homeostatic adaptation of the kidney to K(+) intake.