2006
The connecting tubule is the main site of the furosemide-induced urinary acidification by the vacuolar H+-ATPase
Kovacikova J, Winter C, Loffing-Cueni D, Loffing J, Finberg K, Lifton R, Hummler E, Rossier B, Wagner C. The connecting tubule is the main site of the furosemide-induced urinary acidification by the vacuolar H+-ATPase. Kidney International 2006, 70: 1706-1716. PMID: 16985514, DOI: 10.1038/sj.ki.5001851.Peer-Reviewed Original ResearchMeSH KeywordsAcid-Base EquilibriumAmilorideAnimalsDiureticsEpithelial Sodium ChannelsFurosemideGene Expression RegulationGene Expression Regulation, EnzymologicHydrochlorothiazideHydrogen-Ion ConcentrationKidney Tubules, CollectingKidney Tubules, DistalMetabolic Clearance RateMiceMice, KnockoutNephronsProton-Translocating ATPasesWater-Electrolyte BalanceConceptsUrinary acidificationRenal clearance experimentsEffect of furosemideNormal urinary acidificationLumen-negative voltageNet acid excretionThick ascending limbFinal urinary acidificationKidney-specific inactivationENaC channelsClearance experimentsAcid excretionMouse modelAscending limbFurosemideDuct cellsProton secretionMiceExact localizationReabsorptionMain siteB1 subunitAlpha subunitTubulesFunctional expression
2005
The B1-subunit of the H+ ATPase is required for maximal urinary acidification
Finberg KE, Wagner CA, Bailey MA, Păunescu T, Breton S, Brown D, Giebisch G, Geibel JP, Lifton RP. The B1-subunit of the H+ ATPase is required for maximal urinary acidification. Proceedings Of The National Academy Of Sciences Of The United States Of America 2005, 102: 13616-13621. PMID: 16174750, PMCID: PMC1224669, DOI: 10.1073/pnas.0506769102.Peer-Reviewed Original ResearchConceptsMaximal urinary acidificationNormal urinary acidificationMetabolic acidosisUrinary acidificationDistal renal tubular acidosisAcid challengeRenal tubular acidosisAcute intracellular acidificationB1 subunitLumen-negative potentialFurosemide infusionTubular acidosisAlkaline urineDistal nephronGreater severityAcidosisMiceLoss of B1Intracellular acidificationApical expressionUrineDuctFurther decreaseIsoformsPlasma membrane
2002
Regulation of the expression of the Cl-/anion exchanger pendrin in mouse kidney by acid-base status
Wagner CA, Finberg KE, Stehberger PA, Lifton RP, Giebisch GH, Aronson PS, Geibel JP. Regulation of the expression of the Cl-/anion exchanger pendrin in mouse kidney by acid-base status. Kidney International 2002, 62: 2109-2117. PMID: 12427135, DOI: 10.1046/j.1523-1755.2002.00671.x.Peer-Reviewed Original ResearchConceptsPendrin-positive cellsAcid-base statusPositive cellsBicarbonate secretionMouse kidneyAcid-base transportKnockout mouse modelProtein expression levelsMetabolic alkalosisDeficient dietExchanger pendrinPendrin expressionMouse modelSensorineural deafnessThyroid glandBicarbonate loadPendred syndromeWestern blottingApical membraneInner earPendrin proteinControl levelsKidneyPendrinProtein levels