2023
High dietary K+ intake inhibits proximal tubule transport
Wang T, Liu T, Xu S, Frindt G, Weinstein A, Palmer L. High dietary K+ intake inhibits proximal tubule transport. American Journal Of Physiology. Renal Physiology 2023, 325: f224-f234. PMID: 37318989, PMCID: PMC10396284, DOI: 10.1152/ajprenal.00013.2023.Peer-Reviewed Original ResearchConceptsGlomerular filtration rateFree-flow micropunctureUrine volumeFractional excretion of Na<sup>+</sup>Proximal tubulesFiltration rateFractional NaNephron segmentsExcretion of Na<sup>+</sup>Dietary K<sup>+</sup>NHE3 protein expressionExchanger isoform 3Increased urine volumeIncreased fractional excretionVolume reabsorptionAbsolute NaKidney functionProtein expressionIsoform 3PT transportAnesthetized animalsReabsorptionWestern blottingRatsExcretionHigh Dietary K Intake Inhibits Proximal Tubule Transport and Reduces GFR
Wang T, Liu T, Xu S, Frindt G, Palmer L, Weinstein A. High Dietary K Intake Inhibits Proximal Tubule Transport and Reduces GFR. Physiology 2023, 38: 5731363. DOI: 10.1152/physiol.2023.38.s1.5731363.Peer-Reviewed Original ResearchGlomerular filtration rateReduced glomerular filtration rateK + excretionProximal tubulesTubular fluidConnecting tubuleUrine volumeTreated ratsNephron segmentsReduction of glomerular filtration rateProximal tubule transportLengths of proximal tubulesDistal nephron segmentsProximal nephron segmentsFree-flow micropunctureNa + absorptionHK intakeIncreased FENaTubule transportFractional deliveryFiltration rateKidney functionIncreased secretionFluid absorptionFITC-inulin
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