2011
Renal outer medullary potassium channel knockout models reveal thick ascending limb function and dysfunction
Wang T. Renal outer medullary potassium channel knockout models reveal thick ascending limb function and dysfunction. Clinical And Experimental Nephrology 2011, 16: 49-54. PMID: 22038261, DOI: 10.1007/s10157-011-0495-0.Peer-Reviewed Original ResearchConceptsThick ascending limbIon transporter expressionRenal outer medullary potassium channelBartter's syndromeInward rectifier potassium channelPotassium channelsSmall-conductance K channelsROMK null miceMedullary thick ascending limbType II Bartter's syndromeSimilar phenotypeMammalian kidneyApical membraneK channelsROMK knockout miceKnockout modelsChannel activityChannel mutationsRenal functionLimb functionNull micePhysiological conditionsSalt wastingTransporter expressionPathophysiological conditionsGENDER DIFFERENCE IN MODULATION OF ANGIOTENSIN II TYPE 2 RECEPTOR (AT2) FUNCTION AND EXPRESSION IN AT1A RECEPTOR‐DEFICIENT MICE
Yan Q, Wan L, Du Z, Gotoh N, Wang T. GENDER DIFFERENCE IN MODULATION OF ANGIOTENSIN II TYPE 2 RECEPTOR (AT2) FUNCTION AND EXPRESSION IN AT1A RECEPTOR‐DEFICIENT MICE. The FASEB Journal 2011, 25: 835.9-835.9. DOI: 10.1096/fasebj.25.1_supplement.835.9.Peer-Reviewed Original ResearchGlomerular filtration rateAT2 receptorsUrine volumeProximal tubulesNull miceAngiotensin II type 2 receptorAT1a-/- miceMale null miceType 2 receptorExpression levelsAT1A+/+ miceAT2 inhibitorENaC expressionAT2 expressionKidneys of maleNatriuretic effectWT miceNa+ excretionRenal functionNa+ absorptionReal-time PCRFemale null micePD123319Renal clearanceFiltration rate
2008
Female ROMK null mice manifest more severe Bartter II phenotype on renal function and higher PGE2 production
Yan Q, Yang X, Cantone A, Giebisch G, Hebert S, Wang T. Female ROMK null mice manifest more severe Bartter II phenotype on renal function and higher PGE2 production. AJP Regulatory Integrative And Comparative Physiology 2008, 295: r997-r1004. PMID: 18579648, PMCID: PMC2536865, DOI: 10.1152/ajpregu.00051.2007.Peer-Reviewed Original ResearchConceptsROMK null miceFemale null miceNull miceRenal functionSurvival rateExtent of hydronephrosisDegree of hydronephrosisSeverity of hydronephrosisHigher PGE2 productionHydronephrotic miceLower GFRSyndrome pathophysiologyNg/24 hAcid-base parametersFemale micePGE2 productionHydronephrosisHigher survival rateMiceExcretionSignificant differencesUrinaryMalesSexPossible mechanismMouse model of type II Bartter's syndrome. I. Upregulation of thiazide-sensitive Na-Cl cotransport activity
Cantone A, Yang X, Yan Q, Giebisch G, Hebert SC, Wang T. Mouse model of type II Bartter's syndrome. I. Upregulation of thiazide-sensitive Na-Cl cotransport activity. American Journal Of Physiology. Renal Physiology 2008, 294: f1366-f1372. PMID: 18385266, DOI: 10.1152/ajprenal.00608.2007.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAmilorideAnimalsBartter SyndromeCation Transport ProteinsChloridesDisease Models, AnimalDiureticsEpithelial Sodium ChannelsFemaleFurosemideGlomerular Filtration RateHydrochlorothiazideLoop of HenleMaleMiceMice, Mutant StrainsPotassium Channels, Inwardly RectifyingPregnancySodiumSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 1Up-RegulationConceptsThick ascending limbExcretion rateWhole kidney glomerular filtration rateKidney glomerular filtration rateFractional excretion rateFurosemide-induced incrementsGlomerular filtration rateType II Bartter's syndromeHyperprostaglandin E syndromeEffect of furosemideDistal nephron segmentsDistal convoluted tubuleExaggerated natriuresisROMK null miceNa excretionFiltration rateRenal saltAbsolute excretionBartter's syndromeE syndromeMouse modelClearance studiesConvoluted tubulesAscending limbNull miceMouse model of type II Bartter's syndrome. II. Altered expression of renal sodium- and water-transporting proteins
Wagner CA, Loffing-Cueni D, Yan Q, Schulz N, Fakitsas P, Carrel M, Wang T, Verrey F, Geibel JP, Giebisch G, Hebert SC, Loffing J. Mouse model of type II Bartter's syndrome. II. Altered expression of renal sodium- and water-transporting proteins. American Journal Of Physiology. Renal Physiology 2008, 294: f1373-f1380. PMID: 18322017, DOI: 10.1152/ajprenal.00613.2007.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAnimalsBartter SyndromeCarrier ProteinsCation Transport ProteinsDinoprostoneDisease Models, AnimalEpithelial Sodium ChannelsKidney Tubules, DistalKidney Tubules, ProximalLoop of HenleMiceMice, Mutant StrainsPotassium Channels, Inwardly RectifyingReverse Transcriptase Polymerase Chain ReactionSodiumSodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersSodium-Phosphate Cotransporter Proteins, Type IIaSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 1Up-RegulationWaterConceptsThick ascending limbBartter's syndromeBartter-like phenotypeType II Bartter's syndromeWild-type miceAntenatal Bartter syndromeWild-type littermatesROMK null micePlasma aldosteroneMaternal polyhydramniosRenal sodiumVolume depletionRenal tubulopathyMouse modelSemiquantitative immunoblottingProximal tubulesAscending limbKidney homogenatesSyndromeHenle's loopNull miceDCT cellsWater transport proteinsCompensatory mechanismsMice
2006
LOWER GFR CAUSED BY REDUCTION OF FUNCTIONAL NEPHRONS IN ROMK TYPE II BARTTER’S MICE
Yan Q, Zhang J, Hebert S, Giebisch G, Wang T. LOWER GFR CAUSED BY REDUCTION OF FUNCTIONAL NEPHRONS IN ROMK TYPE II BARTTER’S MICE. The FASEB Journal 2006, 20: a408-a408. DOI: 10.1096/fasebj.20.4.a408.Peer-Reviewed Original ResearchROMK null miceNull miceKidneys of wild-typeReduction of nephron numberType II Bartter syndromeROMK knockout miceIncreased renin expressionPlasma aldosterone concentrationWild-type miceDistal nephron segmentsSingle nephron GFRWild-typeRenal clearance experimentsRenal Na+Bartter's syndromeUrine outputNephron numberAldosterone concentrationNephron GFRRenin expressionROMKKnockout miceKnockout kidneysNephron segmentsAscending limb
2004
NHE2‐mediated bicarbonate reabsorption in the distal tubule of NHE3 null mice
Bailey MA, Giebisch G, Abbiati T, Aronson PS, Gawenis LR, Shull GE, Wang T. NHE2‐mediated bicarbonate reabsorption in the distal tubule of NHE3 null mice. The Journal Of Physiology 2004, 561: 765-775. PMID: 15604231, PMCID: PMC1665379, DOI: 10.1113/jphysiol.2004.074716.Peer-Reviewed Original ResearchConceptsBicarbonate excretionDistal tubulesBicarbonate reabsorptionNHE3 null miceBicarbonate loadEarly distal tubule fluidNull miceNephron segmentsVivo micropunctureDistal tubule fluidProximal tubule bicarbonate reabsorptionRenal clearance experimentsUrinary bicarbonate excretionGlomerular filtration rateDistal nephron segmentsUrinary bicarbonate lossRat distal tubulesDistal bicarbonate reabsorptionExcretion of bicarbonateMetabolic acidosisFiltration rateVivo microperfusionClearance experimentsReabsorption capacityMicroperfusion experimentsRenal and intestinal transport defects in Slc26a6-null mice
Wang Z, Wang T, Petrovic S, Tuo B, Riederer B, Barone S, Lorenz JN, Seidler U, Aronson PS, Soleimani M. Renal and intestinal transport defects in Slc26a6-null mice. American Journal Of Physiology - Cell Physiology 2004, 288: c957-c965. PMID: 15574486, DOI: 10.1152/ajpcell.00505.2004.Peer-Reviewed Original ResearchConceptsWild-type miceProximal tubulesSlc26a6-null miceHCO3- secretionKidney proximal tubulesApical membrane ClNull miceBaseline rateNormal blood pressureCl-/formate exchangeBlood pressureKidney functionElectrolyte profileMucosal tissuesIntestinal physiologyUssing chambersSmall intestineMiceFluid absorptionNaCl absorptionStatistical significanceCl-/HCO3NaCl transportDuodenumTubules
2003
ROMK is required for expression of the 70-pS K channel in the thick ascending limb
Lu M, Wang T, Yan Q, Wang W, Giebisch G, Hebert SC. ROMK is required for expression of the 70-pS K channel in the thick ascending limb. American Journal Of Physiology. Renal Physiology 2003, 286: f490-f495. PMID: 14600033, DOI: 10.1152/ajprenal.00305.2003.Peer-Reviewed Original ResearchConceptsThick ascending limbBartter's syndromeK dietK channelsAscending limbChannel activityApical K channelsFunctional expressionHypokalemic alkalosisTAL cellsNull miceSK activityHeterozygous miceHeterogeneous disorderMicePotassium recyclingROMKFunction mutationsSyndromeCritical subunitApical conductanceSalt absorptionLimbDietExpression
2002
Absence of Small Conductance K+ Channel (SK) Activity in Apical Membranes of Thick Ascending Limb and Cortical Collecting Duct in ROMK (Bartter's) Knockout Mice*
Lu M, Wang T, Yan Q, Yang X, Dong K, Knepper MA, Wang W, Giebisch G, Shull GE, Hebert SC. Absence of Small Conductance K+ Channel (SK) Activity in Apical Membranes of Thick Ascending Limb and Cortical Collecting Duct in ROMK (Bartter's) Knockout Mice*. Journal Of Biological Chemistry 2002, 277: 37881-37887. PMID: 12130653, PMCID: PMC4426997, DOI: 10.1074/jbc.m206644200.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsBartter SyndromeBase SequenceCell MembraneDisease Models, AnimalDNA PrimersGene Expression RegulationGenotypeHumansKidneyKidney CortexKidney Tubules, CollectingMiceMice, KnockoutPotassium ChannelsPotassium Channels, Calcium-ActivatedPotassium Channels, Inwardly RectifyingPotassium ChlorideSmall-Conductance Calcium-Activated Potassium ChannelsSurvival AnalysisConceptsThick ascending limbSK channel activityROMK null miceBartter's syndromeNull miceSK channelsAscending limbChannel activityExtracellular volume depletionROMK geneCortical collecting ductsWild-type littermatesAbsorption/secretionROMK knockout miceNull mice exhibitPatch-clamp analysisSmall conductanceSignificant hydronephrosisRenal morphologyVolume depletionKnockout miceMice exhibitSyndromeCollecting ductsNaCl reabsorption
1999
Mechanism of proximal tubule bicarbonate absorption in NHE3 null mice
Wang T, Yang C, Abbiati T, Schultheis P, Shull G, Giebisch G, Aronson P. Mechanism of proximal tubule bicarbonate absorption in NHE3 null mice. American Journal Of Physiology 1999, 277: f298-f302. PMID: 10444585, DOI: 10.1152/ajprenal.1999.277.2.f298.Peer-Reviewed Original Research