WNK kinases and blood pressure control

Abstract

The WNK (With No K-Lysine) family of proteins is widely expressed and has been shown to promote blood pressure homeostasis through a variety of mechanisms. Members of this family have been reported to affect sodium/chloride cotransporters, sodium/potassium/chloride cotransporters, potassium/chloride cotransporters, the renal outer medullary potassium channel, and the epithelial sodium channel, directly and indirectly. Mutations in WNK1 and WNK4 were shown to cause pseudohypoaldosteronism type II, a Mendelian disorder characterized by hypertension, hyperkalemia, and acidosis. Because of the complexity of the renal system, it has been difficult to completely define the role of these kinases in kidney function. This article reviews current knowledge of the role of these proteins in ion homeostasis and volume control.