Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3885097 | Kidney International | 2013 | 4 Pages |
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.
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Authors
Alicia A. McDonough, Jang H. Youn,