Multigene kinase network, kidney transport, and salt in essential hypertension

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Abstract

Evidence is mounting that a multi-gene kinase network is central to the regulation of renal Na + and K + excretion and that aberrant signaling through the pathway can result in renal sodium retention and hypertension (HTN). The kinase network minimally includes the Ste20-related proline-alanine-rich kinase (SPAK), the with-no-lysine kinases (WNKs), WNK4 and WNK1, and their effectors, the thiazide-sensitive NaCl cotransporter and the potassium secretory channel, ROMK. Available evidence indicates that the kinase network normally functions as a switch to change the mineralocorticoid hormone response of the kidney to either conserve sodium or excrete potassium, depending on whether aldosterone is induced by a change in dietary sodium or potassium. Recently, common genetic variants in the SPAK gene have been identified as HTN susceptibility factors in the general population, suggesting that altered WNK-SPAK signaling plays an important role in essential HTN. Here, we highlight recent breakthroughs in this emerging field and discuss areas of consensus and uncertainty. © 2010 International Society of Nephrology.

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Welling, P. A., Chang, Y. P. C., Delpire, E., & Wade, J. B. (2012, June 2). Multigene kinase network, kidney transport, and salt in essential hypertension. Kidney International. Nature Publishing Group. https://doi.org/10.1038/ki.2010.103

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