2016
Hydronephrosis and Urinary Bladder Hypertrophy in ROMK Bartter's Mouse
Kim J, Guo X, Hu H, Xu S, Wang T. Hydronephrosis and Urinary Bladder Hypertrophy in ROMK Bartter's Mouse. The FASEB Journal 2016, 30 DOI: 10.1096/fasebj.30.1_supplement.1224.30.Peer-Reviewed Original ResearchThickness of urotheliumKO miceROMK expressionBladder capacityBladder weightWT miceKnockout miceRenal outer medullary potassium channelLuminal membraneROMK knockout miceUrinary bladder hypertrophyLow K intakeWestern blottingLow potassium dietSmooth muscle layerMonths of ageNormal KBladder hypertrophyDetrusor muscleMouse bladderBartter's syndromePotassium dietK intakeROMKUrinary bladder
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, 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 loopSyndrome