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 conditions
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, 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
2003
Inhibition of heme oxygenase decreases sodium and fluid absorption in the loop of Henle
Wang T, Sterling H, Shao W, Yan Q, Bailey M, Giebisch G, Wang W. Inhibition of heme oxygenase decreases sodium and fluid absorption in the loop of Henle. American Journal Of Physiology. Renal Physiology 2003, 285: f484-f490. PMID: 12890663, DOI: 10.1152/ajprenal.00135.2003.Peer-Reviewed Original ResearchConceptsLoop of HenleHigh K+K+ channelsApical 70-pS K+ channelRegulation of Na+ transportNa+ transportFluid absorptionApical K+ channelsIn vivo microperfusionInhibition of HORenal sodium excretionGlomerular filtration rateHO-2 expressionInhibitor of HORenal clearance studiesHK ratsHO-2K+ recyclingNa+ absorptionUrinary Na+Sodium excretionChromium mesoporphyrinRat chowWestern blot analysisFiltration rateThe 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(+
2001
Role of NHE isoforms in mediating bicarbonate reabsorption along the nephron
Wang T, Hropot M, Aronson P, Giebisch G. Role of NHE isoforms in mediating bicarbonate reabsorption along the nephron. American Journal Of Physiology. Renal Physiology 2001, 281: f1117-f1122. PMID: 11704563, DOI: 10.1152/ajprenal.2001.281.6.f1117.Peer-Reviewed Original ResearchConceptsLoop of HenleHOE 694Proximal tubulesAddition of ethylisopropylamilorideDistal convoluted tubuleBicarbonate reabsorptionConvoluted tubulesSitu microperfusionRat kidneySignificant inhibitionNHE isoformsHenlePredominant isoformTubulesNHE3Functional roleInhibitionNHE2Apical membraneIsoformsApical isoformKidneyMicroperfusionEthylisopropylamilorideNephron
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