2018
Potassium conservation is impaired in mice with reduced renal expression of Kir4.1
Malik S, Lambert E, Zhang J, Wang T, Clark H, Cypress M, Goldman B, Porter GA, Pena S, Nino W, Gray D. Potassium conservation is impaired in mice with reduced renal expression of Kir4.1. American Journal Of Physiology. Renal Physiology 2018, 315: f1271-f1282. PMID: 30110571, PMCID: PMC6293297, DOI: 10.1152/ajprenal.00022.2018.Peer-Reviewed Original ResearchMeSH KeywordsAlkalosisAnimalsAquaporin 3Gene Knockdown TechniquesGenotypeHypercalcemiaHyperkalemiaHypernatremiaKidney Concentrating AbilityMice, Inbred C57BLMice, KnockoutNephronsPhenotypePhosphorylationPotassium Channels, Inwardly RectifyingPotassium, DietaryRenal ReabsorptionSolute Carrier Family 12, Member 3ConceptsMg-free dietSevere urinary concentrating defectReduced renal expressionRenal K wastingSeSAME/EAST syndromeDistal convoluted tubuleKir4.1 protein expressionWild-type miceUrinary concentrating defectCre-LoxP methodologyAquaporin 3 expressionRelative hypercalcemiaRenal expressionPotassium conservationMetabolic alkalosisNCC expressionChannel Kir4.1Distal nephronKnockout miceConvoluted tubulesCotransporter expressionEAST syndromeHypokalemiaMiceReduced expression
2011
Differential regulation of ROMK (Kir1.1) in distal nephron segments by dietary potassium
Wade JB, Fang L, Coleman RA, Liu J, Grimm PR, Wang T, Welling PA. Differential regulation of ROMK (Kir1.1) in distal nephron segments by dietary potassium. American Journal Of Physiology. Renal Physiology 2011, 300: f1385-f1393. PMID: 21454252, PMCID: PMC3119145, DOI: 10.1152/ajprenal.00592.2010.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsBlotting, WesternMiceMice, KnockoutNephronsPotassium Channels, Inwardly RectifyingPotassium, DietaryConceptsDistal nephronDistal nephron segmentsRenal K secretionROMK knockout miceDietary potassiumExtent of expressionKnockout miceK secretionROMK expressionNephron segmentsNew antibodiesApical labelingPhysiological stimuliNephronROMKAntibodiesROMK channelsApical expressionChannel localizationChannel functionDifferential regulationLarge increaseDCT2Different regulatory mechanismsExtensive pattern
2006
Maxi-K channels contribute to urinary potassium excretion in the ROMK-deficient mouse model of Type II Bartter's syndrome and in adaptation to a high-K diet
Bailey M, Cantone A, Yan Q, MacGregor G, Leng Q, Amorim J, Wang T, Hebert S, Giebisch G, Malnic G. Maxi-K channels contribute to urinary potassium excretion in the ROMK-deficient mouse model of Type II Bartter's syndrome and in adaptation to a high-K diet. Kidney International 2006, 70: 51-59. PMID: 16710355, DOI: 10.1038/sj.ki.5000388.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAnimalsBartter SyndromeBiological TransportDietDisease Models, AnimalHypokalemiaKidney Tubules, DistalLarge-Conductance Calcium-Activated Potassium ChannelsLoop of HenleMiceMice, Mutant StrainsPeptidesPotassiumPotassium Channels, Inwardly RectifyingPotassium, DietaryConceptsCortical collecting ductLate distal tubuleType II Bartter syndromeRenal potassium wastingMaxi-K channelsPotassium secretionDistal tubulesBartter's syndromePotassium wastingPotassium excretionIberiotoxin (IBTX)-sensitiveRenal potassium lossSalt-wasting disorderUrinary potassium excretionWild-type miceRenal potassium excretionFree-flow micropunctureDistal convoluted tubuleIncreased renal potassium excretionHigh-K dietLoop of HenleROMK-deficientPersistent hypokalemiaROMK channelsMaxi-K