2016
Potassium Channelopathies and Gastrointestinal Ulceration
Han J, Lee SH, Giebisch G, Wang T. Potassium Channelopathies and Gastrointestinal Ulceration. Gut And Liver 2016, 10: 881-889. PMID: 27784845, PMCID: PMC5087926, DOI: 10.5009/gnl15414.Peer-Reviewed Original ResearchConceptsPotassium channelsGI tractPotassium channelopathiesAdenosine triphosphate-sensitive potassium channel openerTriphosphate-sensitive potassium channel openerNonsteroidal anti-inflammatory drugsAntianginal drug nicorandilAnti-inflammatory drugsPotassium channel openersOccurrence of ulcerationPotassium channel activityLong-term useRegulation of secretionGastrointestinal ulcerationUlcerative colitisPeptic ulcerationChannel openersGastric acidGastrointestinal tractUlcerationDifferent biological actionsTransporter inhibitorsAnal regionPotassium homeostasisTract
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 absorptionLimbDietExpression
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 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