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Mutations in a recently discovered family of protein kinases are responsible for an autosomal-dominant form of inherited hypertension, known as Gordon’s syndrome or pseudohypoaldosteronism type II (PHAII).1 The phenotype also includes hyperkalemia and hyperchloremic metabolic acidosis.1 The name of this kinase family is WNK (with no lysine [K]) because of the absence of a lysine in subdomain II of the enzymes.2 WNK1 and WNK4 , located in human chromosomes 12 and 17, respectively, are predominantly expressed in the distal convoluted tubules and the collecting ducts of the kidney.1Article p 3423 In vitro, wild-type WNK4 inhibits the thiazide-sensitive sodium chloride cotransporter (NCCT)3,4 and the renal outer medullary potassium ion channel (ROMK),5 but increases paracellular chloride permeability.6 Some WNK4 mutations identified in PHAII behave as a loss of function for the NCCT inhibition3,4,7 but as a gain of function for the inhibition of ROMK,5,7 and further stimulate paracellular chloride transport.6,8 These effects of WNK4 mutations fit well with the proposed mechanisms for the development of hypertension and electrolyte abnormalities in PHAII. Furthermore, in vitro, WNK1 counteracts the inhibition of NCCT by WNK4 4 and activates the serum- and glucocorticoid-inducible protein kinase ( SGK1 ), which in turn stimulates the epithelial sodium channel (ENaC).9 The observation that heterozygous WNK1 -deficient mice …

Association of Blood Pressure With Genetic Variation in WNK Kinases in a White European Population