title: Need to quickly excrete K(+)? Turn off NCC.
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.
authors: Department of Cell and Neurobiology, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA. mcdonoug@usc.edu
authors: Alicia A
authors: AA
authors: McDonough
authors: Jang H
authors: JH
authors: Youn
mesh_terms: D000818:Animals; D005260:Female; D007668:Kidney / Q000378:metabolism*; D008297:Male; D017419:Potassium, Dietary / Q000097:blood*; D011955:Receptors, Drug / Q000378:metabolism*; D064486:Solute Carrier Family 12, Member 3; D027981:Symporters / Q000378:metabolism*
chemical_list: D017419:Potassium, Dietary; D011955:Receptors, Drug; C578875:Slc12a3 protein, mouse; D064486:Solute Carrier Family 12, Member 3; D027981:Symporters
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