Journal article
Mechanisms of disease: WNK-ing at the mechanism of salt-sensitive hypertension
Nature clinical practice. Nephrology, Vol.3(11), pp.623-630
11/2007
DOI: 10.1038/ncpneph0638
PMID: 17957199
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.
Details
- Title: Subtitle
- Mechanisms of disease: WNK-ing at the mechanism of salt-sensitive hypertension
- Creators
- Chou-Long Huang - Division of Nephrology, UT Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-8856, USA. chou-long.huang@utsouthwestern.eduElizabeth Kuo
- Resource Type
- Journal article
- Publication Details
- Nature clinical practice. Nephrology, Vol.3(11), pp.623-630
- DOI
- 10.1038/ncpneph0638
- PMID
- 17957199
- ISSN
- 1745-8331
- eISSN
- 1745-8331
- Grant note
- DK-59530 / NIDDK NIH HHS DK-54368 / NIDDK NIH HHS
- Language
- English
- Date published
- 11/2007
- Academic Unit
- Nephrology; Internal Medicine
- Record Identifier
- 9984094325602771
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