2008
Mouse 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
2007
Transgenic RNAi Depletion of Claudin-16 and the Renal Handling of Magnesium*
Hou J, Shan Q, Wang T, Gomes A, Yan Q, Paul D, Bleich M, Goodenough D. Transgenic RNAi Depletion of Claudin-16 and the Renal Handling of Magnesium*. Journal Of Biological Chemistry 2007, 282: 17114-17122. PMID: 17442678, DOI: 10.1074/jbc.m700632200.Peer-Reviewed Original ResearchConceptsClaudin-16Tight junction proteinsTight junction proteins claudin-16Junction proteinsRenal handlingTight junctionsRenal handling of magnesiumRenal wasting of magnesiumParacellular ion reabsorptionHandling of magnesiumKnock-downFamilial hypomagnesemiaRenal functionElectrolyte disordersCation channelsTarget of drug developmentAscending limbMouse modelFHHNCParacellular cation channelsControl of ion homeostasisRenal controlIn vivo analysisIon reabsorptionNephrocalcinosis
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 limbUse of transgenic mice in acid-base balance studies.
Cantone A, Wang T, Pica A, Simeoni M, Capasso G. Use of transgenic mice in acid-base balance studies. Journal Of Nephrology 2006, 19 Suppl 9: s121-7. PMID: 16736435.Peer-Reviewed Original ResearchMeSH KeywordsAcid-Base EquilibriumAcid-Base ImbalanceAnimalsCation Transport ProteinsDisease Models, AnimalDNAGene ExpressionKidney TubulesMembrane ProteinsMiceMice, TransgenicNitric Oxide SynthaseSodium-Bicarbonate SymportersSodium-Hydrogen Exchanger 1Sodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersConceptsNitric oxide synthaseAcid-base statusNa+/H+ exchangeBody acid-base statusTransgenic miceFunction of pendrinProximal tubule transportTransepithelial HCO3- absorptionPotassium-chloride cotransporterEndothelial isoform of nitric oxide synthaseIsoform of nitric oxide synthaseSubunit expression levelsKnockout animal modelsApical NHE3Basolateral NHE1HCO3- absorptionNa+/HCO3- cotransporterNatriuretic responseRegulation of acid-base balanceTubule transportDistal nephronProximal tubulesRenal diseaseChloride channelsAscending limb
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 absorptionLimbDietExpressionThe Effects of the Potassium Channel Opener Minoxidil on Renal Electrolytes Transport in the Loop of Henle
Wang T. The Effects of the Potassium Channel Opener Minoxidil on Renal Electrolytes Transport in the Loop of Henle. Journal Of Pharmacology And Experimental Therapeutics 2003, 304: 833-840. PMID: 12538840, DOI: 10.1124/jpet.102.043380.Peer-Reviewed Original ResearchConceptsLoop of HenleUrine volumeIn vivo microperfusion techniquesCa(2+ATP-sensitive potassium channelsRenal electrolyte transportK channel openerPotassium channel opener minoxidilGlomerular filtration rateApical K(+Fractional Na(+Natriuretic effectAntinatriuretic actionsRenal clearanceFiltration ratePotassium channelsUrinary excretionIncreased fluidAscending limbIntravenous injectionBlood pressureMicroperfusion techniqueHenlePerfusion fluidDecreased Na(+
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
1995
Effects of a novel KATP channel blocker on renal tubule function and K channel activity.
Wang T, Wang W, Klein-Robbenhaar G, Giebisch G. Effects of a novel KATP channel blocker on renal tubule function and K channel activity. Journal Of Pharmacology And Experimental Therapeutics 1995, 273: 1382-9. PMID: 7791111.Peer-Reviewed Original ResearchConceptsCortical collecting tubuleKATP channel blockerChannel blockersPotassium recyclingPotassium secretionAscending limbATP-sensitive potassium channelsActivation of KATPApical potassium conductanceReduced potassium secretionK channel activityRenal tubule functionLoop of HenleModulate NaCl reabsorptionPotassium conductanceSodium reabsorptionK secretionApical membranePrincipal cellsTubule functionPotassium channelsKATPBlockersReabsorptionEffects of Glyburide on Renal Tubule Transport and Potassium-Channel Activity
Wang T, Wang W, Klein-Robbenhaar G, Giebisch G. Effects of Glyburide on Renal Tubule Transport and Potassium-Channel Activity. Kidney & Blood Pressure Research 1995, 18: 169-182. PMID: 7481068, DOI: 10.1159/000173914.Peer-Reviewed Original ResearchConceptsK channelsApical membraneInhibition of K secretionApical K channelsRenal tubule transportCortical collecting tubuleK channel activityPatch-clamp techniquePotassium channel activityEffect of glyburideTubule transportK secretionRenal clearanceElectrolyte excretionPotassium channelsTransport of NaAscending limbGlyburideInhibit transportK recyclingKaliuresisHenleMicroperfusionTubulesExcretion