Hypertension Research Today is a free monthly online journal that collates and summarizes the latest research about Hypertension, including details on symptoms, diagnosis, diet, treatment, causes.

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

Huang CL, Kuo E

Division of Nephrology, UT Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-8856, USA. chou-long.huang@utsouthwestern.edu

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.

Published 24 October 2007 in Nat Clin Pract Nephrol, 3(11): 623-30.
Full-text of this article is available online (may require subscription).

© 2004-2008 Hypertension Research Today. All Rights Reserved.