WNK kinases and blood pressure control
SL Deaton, S Sengupta, MH Cobb - Current hypertension reports, 2009 - Springer
SL Deaton, S Sengupta, MH Cobb
Current hypertension reports, 2009•SpringerAbstract The WNK (W ith N o 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 …
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 …
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.
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