2021
Sex difference in kidney electrolyte transport III: Impact of low K intake on thiazide-sensitive cation excretion in male and female mice
Xu S, Li J, Yang L, Wang CJ, Liu T, Weinstein AM, Palmer LG, Wang T. Sex difference in kidney electrolyte transport III: Impact of low K intake on thiazide-sensitive cation excretion in male and female mice. Pflügers Archiv - European Journal Of Physiology 2021, 473: 1749-1760. PMID: 34455480, PMCID: PMC8528772, DOI: 10.1007/s00424-021-02611-5.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCationsDiureticsFemaleGlomerular Filtration RateIon TransportKidney Tubules, DistalMaleMiceMice, Inbred C57BLNephronsPotassium Channels, Inwardly RectifyingSex CharacteristicsSodiumSolute Carrier Family 12, Member 3ThiazidesConceptsGlomerular filtration rateFemale miceUrine volumeNaCl cotransporterLow K intakeMeasurement of functionSex differencesNatriuretic responseFractional excretionK intakeTransport protein expressionFiltration rateNCC abundanceNCC expressionRenal clearanceDistal nephronLK dietCation excretionPlasma KNCC proteinNKCC2 expressionWestern blottingProtein expressionMiceFENa
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 ResearchMeSH KeywordsAnimalsKidney Tubules, DistalLoop of HenleMiceMice, KnockoutPotassiumPotassium Channels, Inwardly RectifyingSodium ChlorideSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 1ConceptsThick 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 conditionsDifferential regulation of ROMK (Kir1.1) in distal nephron segments by dietary potassium
Wade JB, Fang L, Coleman RA, Liu J, Grimm PR, Wang T, Welling PA. Differential regulation of ROMK (Kir1.1) in distal nephron segments by dietary potassium. American Journal Of Physiology. Renal Physiology 2011, 300: f1385-f1393. PMID: 21454252, PMCID: PMC3119145, DOI: 10.1152/ajprenal.00592.2010.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsBlotting, WesternMiceMice, KnockoutNephronsPotassium Channels, Inwardly RectifyingPotassium, DietaryConceptsDistal nephronDistal nephron segmentsRenal K secretionROMK knockout miceDietary potassiumExtent of expressionKnockout miceK secretionROMK expressionNephron segmentsNew antibodiesApical labelingPhysiological stimuliNephronROMKAntibodiesROMK channelsApical expressionChannel localizationChannel functionDifferential regulationLarge increaseDCT2Different regulatory mechanismsExtensive pattern
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
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