2018
Regulation of renal Na transporters in response to dietary K
Yang L, Xu S, Guo X, Uchida S, Weinstein AM, Wang T, Palmer LG. Regulation of renal Na transporters in response to dietary K. American Journal Of Physiology. Renal Physiology 2018, 315: f1032-f1041. PMID: 29923764, PMCID: PMC6230734, DOI: 10.1152/ajprenal.00117.2018.Peer-Reviewed Original Research
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
Low Na intake suppresses expression of CYP2C23 and arachidonic acid-induced inhibition of ENaC
Sun P, Lin D, Wang T, Babilonia E, Wang Z, Jin Y, Kemp R, Nasjletti A, Wang W. Low Na intake suppresses expression of CYP2C23 and arachidonic acid-induced inhibition of ENaC. American Journal Of Physiology. Renal Physiology 2006, 291: f1192-f1200. PMID: 16849695, DOI: 10.1152/ajprenal.00112.2006.Peer-Reviewed Original ResearchMeSH Keywords8,11,14-Eicosatrienoic AcidAnimalsArachidonic AcidCytochrome P-450 CYP2J2Cytochrome P-450 Enzyme SystemEpithelial Sodium ChannelsFemaleIon Channel GatingKidney Tubules, CollectingMaleMembrane PotentialsPatch-Clamp TechniquesRatsRats, Sprague-DawleySodium, DietarySpecific Pathogen-Free OrganismsConceptsExpression of CYP2C23Low Na intakeCollecting ductsMS-PPOHEpoxyeicosatrienoic acidsDistal nephronArachidonic acidNa intakeInhibition of CYP epoxygenaseNa transportNa absorptionArachidonic acid-induced inhibitionControl Na dietInhibition of ENaC.Na-deficient dietNormal-Na dietActivation of ENaCEpithelial Na channelPatch-clamp studiesHigh-Na dietIncreased Na absorptionAA-induced inhibitionInhibitory effectENaC activityNa restriction
2003
Expression of ENaC and serum- and glucocorticoid-induced kinase 1 in the rat intestinal epithelium
Coric T, Hernandez N, de la Rosa D, Shao D, Wang T, Canessa CM. Expression of ENaC and serum- and glucocorticoid-induced kinase 1 in the rat intestinal epithelium. AJP Gastrointestinal And Liver Physiology 2003, 286: g663-g670. PMID: 14630642, DOI: 10.1152/ajpgi.00364.2003.Peer-Reviewed Original ResearchMeSH KeywordsAldosteroneAnimalsAntibodies, BlockingAntibody SpecificityBlotting, NorthernCHO CellsColonCricetinaeDNA, ComplementaryEnzyme InductionEpithelial Sodium ChannelsEpitheliumFluorescent Antibody TechniqueImmediate-Early ProteinsIntestinal MucosaNuclear ProteinsPlasmidsProtein Serine-Threonine KinasesRatsRNA, MessengerSignal TransductionSodium ChannelsConceptsDistal colonGlucocorticoid-induced kinase 1Intestinal epitheliumConcentrations of aldosteroneSubunits of ENaCSodium channel activityExpression of ENaCRat intestinal epitheliumKinase 1Aldosterone levelsAldosterone-dependent mannerSingle doseSodium depletionChronic increaseDistal tubulesControl animalsAldosteroneAldosterone inductionRat intestineBasal conditionsColonSodium transportersEpitheliumSites of expressionSGK1