Mechanisms of Disease: WNK-ing at the mechanism of salt-sensitive hypertension

Chou Long Huang, Elizabeth Kuo

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

Potassium deficiency is associated with an increased prevalence of hypertension. Increasing potassium intake lowers blood pressure via an unknown mechanism. WNK (with no lysine) kinases are a novel family of large serine/threonine protein kinases. A large deletion from the first intron of the WNK1 gene results in increased levels of expression of WNK1 and causes Gordon's syndrome, of which hypertension and hyperkalemia are features. WNK1 activates the Na+/Cl- cotransporter NCC and the epithelial Na + channel ENaC, and inhibits the renal K+ channel ROMK. Enhanced Na+ reabsorption and inhibition of K+ secretion resulting from increased WNK1 expression probably contribute to hypertension and hyperkalemia in Gordon's syndrome. Here, we review the role of dietary K + deficiency in the pathogenesis of salt-sensitive hypertension and summarize recent findings indicating that WNK1 might mediate renal Na + retention and hypertension in K+ deficiency.

Original languageEnglish (US)
Pages (from-to)623-630
Number of pages8
JournalNature Clinical Practice Nephrology
Volume3
Issue number11
DOIs
StatePublished - Nov 2007

Fingerprint

Pseudohypoaldosteronism
Salts
Hypertension
Member 3 Solute Carrier Family 12
Potassium Deficiency
Epithelial Sodium Channels
Kidney
Protein-Serine-Threonine Kinases
Introns
Lysine
Potassium
Phosphotransferases
Blood Pressure
Genes

Keywords

  • Dietary potassium intake
  • Gordon's syndrome
  • Potassium deficiency
  • Salt-sensitive hypertension
  • WNK kinase

ASJC Scopus subject areas

  • Nephrology

Cite this

Mechanisms of Disease : WNK-ing at the mechanism of salt-sensitive hypertension. / Huang, Chou Long; Kuo, Elizabeth.

In: Nature Clinical Practice Nephrology, Vol. 3, No. 11, 11.2007, p. 623-630.

Research output: Contribution to journalArticle

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