1998
Converting enzyme inhibition causes hypocitraturia independent of acidosis or hypokalemia
Melnick J, Preisig P, Haynes S, Pak C, Sakhaee K, Alpern R. Converting enzyme inhibition causes hypocitraturia independent of acidosis or hypokalemia. Kidney International 1998, 54: 1670-1674. PMID: 9844143, DOI: 10.1046/j.1523-1755.1998.00150.x.Peer-Reviewed Original ResearchConceptsUrinary citrate excretionCitrate excretionUrinary citrateMetabolic acidosisATP-citrate lyaseEffects of enalaprilRenal citrate metabolismUrine citrate concentrationRenal cortical tissueChronic metabolic acidosisProximal tubular cellsPlasma pHNa/H antiporterAngiotensin IIIntracellular acidosisEnalaprilTubular cellsCitrate lyaseHypokalemiaEnzyme inhibitorsATP citrate lyase activityAcidosisCortical tissueRatsCitrate metabolismDominant negative c-Src inhibits angiotensin II induced activation of NHE3 in OKP cells
Tsuganezawa H, Preisig P, Alpern R. Dominant negative c-Src inhibits angiotensin II induced activation of NHE3 in OKP cells. Kidney International 1998, 54: 394-398. PMID: 9690205, DOI: 10.1046/j.1523-1755.1998.00029.x.Peer-Reviewed Original ResearchConceptsNa/H antiporter activityAngiotensin IIOKP cellsInhibits angiotensin IIVascular smooth muscleTyrosine kinase inhibitorsC-SrcHerbimycin AAntiporter activityNa/H antiporterActivation of NHE3Smooth muscleProximal tubulesPotent stimulatorNHE3 activationRegulation of NHE3Key mediatorKinase inhibitorsClonal cell linesNHE3 activityAntiporter activationCyclic AMPCell linesNHE3Acidosis
1994
Angiotensin II stimulation of Na-H antiporter activity is cAMP independent in OKP cells
Cano A, Miller RT, Alpern RJ, Preisig PA. Angiotensin II stimulation of Na-H antiporter activity is cAMP independent in OKP cells. American Journal Of Physiology 1994, 266: c1603-c1608. PMID: 8023891, DOI: 10.1152/ajpcell.1994.266.6.c1603.Peer-Reviewed Original ResearchConceptsPertussis toxin-sensitive G proteinToxin-sensitive G proteinNa-H antiporter activityAngiotensin IINa-H antiporterOKP cellsAngiotensin II concentrationAngiotensin II receptorsAbsence of IBMXAngiotensin II stimulationG proteinsCyclic monophosphateProximal tubule apical membraneOpossum kidney cellsConcentration-dependent mannerCAMP-independent mechanismM losartanAcute treatmentAT1 receptorII stimulationPertussis toxinII receptorsProximal tubulesCAMP productionStimulatory effect
1993
Cyclic adenosine monophosphate acutely inhibits and chronically stimulates Na/H antiporter in OKP cells.
Cano A, Preisig P, Alpern RJ. Cyclic adenosine monophosphate acutely inhibits and chronically stimulates Na/H antiporter in OKP cells. Journal Of Clinical Investigation 1993, 92: 1632-1638. PMID: 7691881, PMCID: PMC288321, DOI: 10.1172/jci116748.Peer-Reviewed Original ResearchConceptsNa/H antiporter activityRenal Na excretionNa excretionNa/H antiporterOKP cellsH antiporterAntiporter activityAddition of forskolinParathyroid hormoneAngiotensin IIAcute effectsChronic increaseChronic activationCyclic adenosine monophosphateChronic effectsChronic applicationNonspecific effectsPersistent activationPersistent increaseAlpha-adrenergic catecholaminesCell cAMPEndogenous generationAdenosine monophosphateH exposureCell acidification
1991
Regulation of proximal reabsorption by effective arterial blood volume.
Seldin DW, Preisig PA, Alpern RJ. Regulation of proximal reabsorption by effective arterial blood volume. Seminars In Nephrology 1991, 11: 212-9. PMID: 2034926.Peer-Reviewed Original ResearchConceptsEffective arterial blood volumeEffective arterial volumeRenal nerve activityProximal tubular transportAtrial natriuretic factorArterial blood volumeLevels of hormonesRenal hemodynamicsNerve activityDietary NaClAngiotensin IIProximal reabsorptionNatriuretic factorBlood volumeTubular transportProximal tubulesChronic effectsArterial volumeOncotic pressureNorepinephrineHemodynamicsEpinephrineHormoneReabsorption