2009
Chapter 19 The Syndrome of Hypertension and Hyperkalemia (Pseudohypoaldosteronism Type II) WNK Kinases Regulate the Balance Between Renal Salt Reabsorption and Potassium Secretion
Kahle K, Wilson F, Lifton R. Chapter 19 The Syndrome of Hypertension and Hyperkalemia (Pseudohypoaldosteronism Type II) WNK Kinases Regulate the Balance Between Renal Salt Reabsorption and Potassium Secretion. 2009, 313-329. DOI: 10.1016/b978-0-12-449851-8.00019-x.ChaptersRenal potassium secretionLumen-negative potentialPotassium secretionPseudohypoaldosteronism type IINa-Cl cotransporterSalt reabsorptionDistal nephron potassium secretionPotassium channelsRenal outer medullary potassium channelENaC activitySyndrome of hypertensionPotential targetElectrogenic sodium reabsorptionPotassium channel ROMKDistal proton secretionRenal salt reabsorptionBK potassium channelsEpithelial sodium channelMolecular genetic discoveriesSodium reabsorptionWNK kinasesProfound hyperkalemiaImpaired productionMarked impairmentChannel ROMK
2006
WNK3, a kinase related to genes mutated in hereditary hypertension with hyperkalaemia, regulates the K+ channel ROMK1 (Kir1.1)
Leng Q, Kahle KT, Rinehart J, MacGregor GG, Wilson FH, Canessa CM, Lifton RP, Hebert SC. WNK3, a kinase related to genes mutated in hereditary hypertension with hyperkalaemia, regulates the K+ channel ROMK1 (Kir1.1). The Journal Of Physiology 2006, 571: 275-286. PMID: 16357011, PMCID: PMC1796803, DOI: 10.1113/jphysiol.2005.102202.Peer-Reviewed Original ResearchConceptsDistal convoluted tubuleInhibition of ROMK1KCNQ1/KCNE1Renal NaCl reabsorptionEpithelial sodium channelAmiloride-sensitive currentDistal nephronVivo effectsConvoluted tubulesKinase-dependent activationQT syndromeNCC activityNaCl reabsorptionNephron segmentsDuct principal cellsHereditary hypertensionSodium channelsPrincipal cellsII cellsRenal NaClSurface expressionXenopus laevis oocytesHypertensionHomeostatic systemDisease