WNK4, as thiazides, shuts off NaCl reabsorption to stimulate Na/K exchange.
Verrey
Francois
F
Institute of Physiology, University of Zürich, Winterthurerstrasse 190, CH-8057 Zürich, Switzerland. verrey@access.unizh.ch
D000042:Absorption / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D004232:Diuretics; D006801:Humans; D006947:Hyperkalemia / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology; D007686:Kidney Tubules, Distal / Q000378:metabolism*; D051379:Mice; D008822:Mice, Transgenic; D009154:Mutation / Q000235:genetics; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000502:physiology*; D012965:Sodium Chloride / Q000378:metabolism*; D049992:Sodium Chloride Symporters / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology*
D004232:Diuretics; D049992:Sodium Chloride Symporters; D012965:Sodium Chloride; C499024:Prkwnk4 protein, mouse; D017346:Protein Serine-Threonine Kinases; C433806:WNK4 protein, human; D000254:Sodium-Potassium-Exchanging ATPase