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
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, DietaryConceptsLate distal tubuleType II Bartter's syndromePotassium secretionDistal tubulesPotassium excretionRenal potassiumBartter's syndromeUrinary potassium excretionRenal potassium excretionRenal potassium lossFree-flow micropunctureDistal convoluted tubuleWild-type miceLoop of HenleThick ascending limbSalt-wasting disorderPersistent hypokalemiaMaxi-K channelsMouse modelConvoluted tubulesK secretionStationary microperfusionAscending limbHenle's loopSyndromeUse 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 ExchangersConceptsAcid-base statusNitric oxide synthaseTransgenic miceMedullary thick ascending limbProximal tubule transportThick ascending limbSubunit expression levelsPotassium-chloride cotransporterKnockout animal modelsAcid-base balanceKidney regulationTransepithelial HCO3- absorptionNatriuretic responseBlood pressureRenal diseaseOxide synthaseDistal nephronAnimal modelsEndothelial isoformTubule transportBasolateral NHE1Proximal tubulesFunction of pendrinAscending limbHCO3- absorption
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 volumePotassium channel opener minoxidilATP-sensitive potassium channelsChannel opener minoxidilK channel openerGlomerular filtration rateRenal electrolyte transportAddition of minoxidilThick ascending limbVivo microperfusion techniquesAntinatriuretic actionNatriuretic effectBlood pressureUrinary excretionFiltration rateChannel openersIntravenous injectionRenal clearanceAscending limbK cotransporterPerfusion fluidMinoxidilMicroperfusion techniqueHenle
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 ResearchConceptsKATP channel blockerLoop of HenleCortical collecting tubuleThick ascending limbPotassium secretionChannel blockersCollecting tubuleAscending limbPotassium recyclingRenal tubule functionK channel activitySodium reabsorptionTubule functionCl reabsorptionK secretionPotassium conductanceApical potassium conductancePrincipal cellsSecretionChannel activityBlockersHenleReabsorptionLimbRecent studiesEffects 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 ResearchConceptsThick ascending limbRenal tubule transportEffects of glyburideCortical collecting tubuleK channel activityPatch-clamp techniqueApical K channelsPotassium channel activityElectrolyte excretionRenal clearanceK secretionTubule transportCollecting tubuleAscending limbGlyburideApical membraneK channelsK recyclingTransport of NaKaliuresis