title: WNK kinases and essential hypertension.
abstract: OBJECTIVE
  The present review summarizes recent literature and discusses the potential roles of WNKs in the pathogenesis of essential hypertension.
  
  
  RESULTS
  WNKs (with-no-lysine [K]) are a recently discovered family of serine-threonine protein kinases with unusual protein kinase domains. The role of WNK kinases in the control of blood pressure was first revealed by the findings that mutations of two members, WNK1 and WNK4, cause Gordon's syndrome. Laboratory studies have revealed that WNK kinases play important roles in the regulation of sodium and potassium transport. Animal models have been created to unravel the pathophysiology of sodium transport disorders caused by mutations of the WNK4 gene. Potassium deficiency causes sodium retention and increases hypertension prevalence. The expression of WNK1 is upregulated by potassium deficiency, raising the possibility that WNK1 may contribute to salt-sensitive essential hypertension associated with potassium deficiency. Associations of polymorphisms of WNK genes with essential hypertension in the general population have been reported.
  
  
  CONCLUSIONS
  Mutations of WNK1 and WNK4 cause hypertension at least partly by increasing renal sodium retention. The role of WNK kinases in salt-sensitive hypertension within general hypertension is suggested, but future work is required to firmly establish the connection.
authors.affiliation: Department of Medicine, Division of Nephrology, UT Southwestern Medical Center, Dallas, Texas 75390-8856, USA. chou-long.huang@utsouthwestern.edu
authors.forename: Chou-Long
authors.initials: CL
authors.lastname: Huang
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Kuo
authors.forename: Robert D
authors.initials: RD
authors.lastname: Toto
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000235:genetics; D020022:Genetic Predisposition to Disease; D006801:Humans; D006973:Hypertension / Q000139:chemically induced / Q000201:enzymology* / Q000235:genetics / Q000503:physiopathology; D047908:Intracellular Signaling Peptides and Proteins; D015778:Minor Histocompatibility Antigens; D023421:Models, Animal; D009154:Mutation; D011110:Polymorphism, Genetic; D011191:Potassium Deficiency / Q000150:complications / Q000201:enzymology / Q000473:pathology; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D011546:Pseudohypoaldosteronism / Q000201:enzymology / Q000503:physiopathology; D012307:Risk Factors; D015398:Signal Transduction / Q000235:genetics; D017673:Sodium Chloride, Dietary / Q000009:adverse effects; D000076204:WNK Lysine-Deficient Protein Kinase 1; D014882:Water-Electrolyte Balance
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; D015778:Minor Histocompatibility Antigens; D017673:Sodium Chloride, Dietary; D017346:Protein Serine-Threonine Kinases; D000076204:WNK Lysine-Deficient Protein Kinase 1; C498743:WNK1 protein, human; C433806:WNK4 protein, human