Department of Cell and Neurobiology, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA.
Kidney Int. 2013 May;83(5):779-82. doi: 10.1038/ki.2012.468.
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.
膳食钾摄入后,肾脏钾排泄迅速增加,但其中的分子机制在很大程度上尚不清楚。Sorensen 及其同事的研究表明,在小鼠中摄入钾会迅速且近乎完全去磷酸化肾脏远曲小管 NaCl 共转运蛋白,同时伴有钠和钾排泄的增加。这种反应不受醛固酮的影响,可能是肾脏对钾摄入进行急性体内平衡适应的关键组成部分。