2007
Acute tissue-type plasminogen activator release in human microvascular endothelial cells: The roles of Gαq, PLC-β, IP3 and 5,6-epoxyeicosatrienoic acid
Muldowney JA, Painter CA, Sanders-Bush E, Brown NJ, Vaughan DE. Acute tissue-type plasminogen activator release in human microvascular endothelial cells: The roles of Gαq, PLC-β, IP3 and 5,6-epoxyeicosatrienoic acid. Thrombosis And Haemostasis 2007, 97: 263-271. PMID: 17264956, DOI: 10.1160/th05-02-0092.Peer-Reviewed Original ResearchMeSH Keywords8,11,14-Eicosatrienoic AcidAortaBiological FactorsCell ProliferationCells, CulturedDose-Response Relationship, DrugEndothelial CellsEpoprostenolGTP-Binding Protein alpha Subunits, Gq-G11HumansInositol 1,4,5-TrisphosphateIsoenzymesMicrocirculationNitric OxidePhospholipase C betaPotassiumSignal TransductionThrombinTime FactorsTissue Plasminogen ActivatorType C PhospholipasesUmbilical VeinsConceptsT-PA releaseHuman microvascular endothelial cellsMicrovascular endothelial cellsEpoxyeicosatrienoic acidsTissue-type plasminogen activatorTissue-type plasminogen activator releaseEndothelial cellsIP3 receptor antagonistCalcium signalingT-PA antigenRole of GαqPlasminogen activator releaseMS-PPOHPhysiologic releaseCytochrome P450 inhibitorsL-NAMEEET antagonistReceptor antagonistActivator releaseVascular homeostasisNitric oxideProstacyclinPlasminogen activatorEET-methyl esterMicroM concentrationA population-based study in Ghana to investigate inter-individual variation in plasma t-PA and PAI-1.
Williams SM, Stocki S, Jiang L, Brew K, Gordon S, Vaughan DE, Brown NJ, Poku KA, Moore JH. A population-based study in Ghana to investigate inter-individual variation in plasma t-PA and PAI-1. Ethnicity & Disease 2007, 17: 492-7. PMID: 17985503.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1Tissue-type plasminogen activatorInter-individual variationGenetic architectureSignificant genetic componentGenetic analysisGenetic componentPhenotype informationPopulation-based studyPlasma t-PAActivator inhibitor-1Inhibitor-1Unrelated subjectsLarge-scale population-based studyStudy designChronic disease statusSystolic blood pressurePlasminogen activatorRisk of thrombosisProtein
2005
Melanocortin-4 Receptor–Deficient Mice Are Not Hypertensive or Salt-Sensitive Despite Obesity, Hyperinsulinemia, and Hyperleptinemia
Ma J, Albornoz F, Yu C, Byrne DW, Vaughan DE, Brown NJ. Melanocortin-4 Receptor–Deficient Mice Are Not Hypertensive or Salt-Sensitive Despite Obesity, Hyperinsulinemia, and Hyperleptinemia. Hypertension 2005, 46: 326-332. PMID: 15998706, DOI: 10.1161/01.hyp.0000174327.53863.86.Peer-Reviewed Original ResearchMeSH KeywordsAdultCross-Over StudiesDiureticsDouble-Blind MethodElectrolytesFemaleFibrinolysisHemodynamicsHumansHydrochlorothiazideHypertensionMaleMiddle AgedMineralocorticoid Receptor AntagonistsPlasminogen Activator Inhibitor 1PotassiumReceptors, MineralocorticoidRenin-Angiotensin SystemSodium Chloride Symporter InhibitorsSpironolactoneTriamtereneConceptsPAI-1 antigenMineralocorticoid receptor antagonismHypertensive subjectsPAI-1 responseTissue-type plasminogen activatorAldosterone systemNormotensive subjectsFibrinolytic balanceReceptor antagonismMelanocortin 4 receptor-deficient micePlasminogen activator inhibitor-1 (PAI-1) concentrationsEffect of spironolactoneReceptor-deficient miceEffect of triamtereneBlood pressureSerum potassiumTreatment groupsEffects of activationSpironolactonePAI-1Plasminogen activatorAntigenTriamtereneRegression analysisSubjects
2002
The Renin-Angiotensin-Aldosterone System and Fibrinolysis in Progressive Renal Disease
Brown NJ, Vaughan DE, Fogo AB. The Renin-Angiotensin-Aldosterone System and Fibrinolysis in Progressive Renal Disease. Seminars In Nephrology 2002, 22: 399-406. PMID: 12224047, DOI: 10.1053/snep.2002.34725.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1Renal diseaseAldosterone systemProgressive renal diseaseFinal common pathwayActivator inhibitor-1Extracellular matrix accumulationPAI-1 expressionInitiating injuryRenal failureRenin-AngiotensinInterstitial fibrosisClinical managementMajor physiologic inhibitorAnimal modelsProduction of plasminFibrosisMatrix accumulationPlasminogen activatorPhysiologic inhibitorInhibitor-1Common pathwayDiseaseInjuryRAASComparative Effects of Estrogen and Angiotensin-Converting Enzyme Inhibition on Plasminogen Activator Inhibitor-1 in Healthy Postmenopausal Women
Brown NJ, Abbas A, Byrne D, Schoenhard JA, Vaughan DE. Comparative Effects of Estrogen and Angiotensin-Converting Enzyme Inhibition on Plasminogen Activator Inhibitor-1 in Healthy Postmenopausal Women. Circulation 2002, 105: 304-309. PMID: 11804984, DOI: 10.1161/hc0302.102570.Peer-Reviewed Original ResearchMeSH KeywordsAldosteroneAngiotensin IIAngiotensin-Converting Enzyme InhibitorsBlood PressureCardiovascular DiseasesCross-Over StudiesDrug Therapy, CombinationEstradiolEstrogen Replacement TherapyEstrogens, Conjugated (USP)FemaleHumansMiddle AgedPlasminogen Activator Inhibitor 1Polymorphism, GeneticPostmenopauseRamiprilReninSingle-Blind MethodTissue Plasminogen ActivatorConceptsHealthy postmenopausal womenPAI-1 4G/5G genotypePlasma renin activityPostmenopausal womenPAI-1 concentrationsACE inhibitionTissue plasminogen activatorConjugated estrogensPAI-1G genotypeRenin activityAngiotensin IIPlasminogen activator inhibitor-1 (PAI-1) concentrationsAngiotensin-Converting Enzyme InhibitionPAI-1 antigen concentrationsPlasminogen activatorConjugated equine estrogensEffects of estrogenPlasminogen activator inhibitor-1Activator inhibitor-1Combination estrogenClinical outcomesEquine estrogensCombined therapyCrossover treatmentAldosterone and PAI-1: implications for renal injury.
Brown NJ, Vaughan DE, Fogo AB. Aldosterone and PAI-1: implications for renal injury. Journal Of Nephrology 2002, 15: 230-5. PMID: 12113592.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1Activator inhibitor-1Renal injuryAnimal modelsInhibitor-1Aldosterone receptor antagonismPlasminogen activator inhibitor-1 expressionExtracellular matrix accumulationPAI-1 expressionMajor physiological inhibitorRenal diseaseAngiotensin IIReceptor antagonismClinical managementAldosteroneProduction of plasminPAI-1FibrosisMatrix accumulationPlasminogen activatorInjuryPhysiological inhibitorVivoExpressionDisease
1999
Role of Angiotensin II in Coagulation and Fibrinolysis
Brown N, Vaughan D. Role of Angiotensin II in Coagulation and Fibrinolysis. Heart Failure Reviews 1999, 3: 193-198. DOI: 10.1023/a:1009757416302.Peer-Reviewed Original ResearchAntithrombotic effectAngiotensin type 1 receptor antagonistType 1 receptor antagonistVascular fibrinolytic balanceRenin-angiotensin systemTissue plasminogen activatorHypertensive patientsInhibitor PAI-1Angiotensin IIFibrinolytic balanceReceptor antagonistVasculoprotective propertiesPlatelet functionEnzyme inhibitorsPAI-1Plasminogen activatorMultiple mechanismsFibrinolysisSubstantial evidenceRecent studiesAngiotensinPatientsProstanoidsAntagonist
1997
Plasminogen actiwator inhibitor type 1 in diabetes and hypertension
Litchfield W, Brown N, Vaughan D. Plasminogen actiwator inhibitor type 1 in diabetes and hypertension. Current Opinion In Endocrinology Diabetes And Obesity 1997, 4: 233-238. DOI: 10.1097/00060793-199706000-00009.Peer-Reviewed Original ResearchCardiovascular riskPAI-1Inhibitor type 1Type 1Elevated levelsIncreased cardiovascular riskRenin-angiotensin systemEndogenous fibrinolytic systemPlasminogen activator inhibitor type 1Activator inhibitor type 1Tissue plasminogen activatorHypertensive patientsEssential hypertensionMyocardial infarctionCardiovascular diseaseFibrinolytic systemHypertensionPlasminogen activatorStrong associationIncidenceRiskPrimary inhibitorHyperinsulinemiaHypertriglyceridemiaInfarctionSelective Stimulation of Tissue-Type Plasminogen Activator (t-PA) In Vivo by Infusion of Bradykinin
Brown N, Nadeau J, Vaughan D. Selective Stimulation of Tissue-Type Plasminogen Activator (t-PA) In Vivo by Infusion of Bradykinin. Thrombosis And Haemostasis 1997, 77: 522-525. PMID: 9066005, DOI: 10.1055/s-0038-1656000.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAngiotensin-Converting Enzyme InhibitorsAntihypertensive AgentsBlood PressureBradykininCaptoprilFemaleHumansHypertensionIsoquinolinesMalePlasminogen Activator Inhibitor 1QuinaprilRandomized Controlled Trials as TopicTetrahydroisoquinolinesTissue Plasminogen ActivatorConceptsT-PA antigen levelsTissue-type plasminogen activatorMean arterial pressureT-PA levelsAntigen levelsPAI-1 antigen levelsInfusion of bradykininSympathetic nervous systemEffect of bradykininTissue-type plasminogen activator secretionHypertensive patientsHemodynamic effectsArterial pressurePlasminogen activator secretionAngiotensin IIAnimal modelsPotent stimulusNervous systemPAI-1ACEIBradykininBradykinin resultsSelective stimulationPlasminogen activatorSignificant decrease
1996
The Renin-Angiotensin and Fibrinolytic Systems Co-Conspirators in the Pathogenesis of Ischemic Cardiovascular Disease
Brown N, Vaughan D. The Renin-Angiotensin and Fibrinolytic Systems Co-Conspirators in the Pathogenesis of Ischemic Cardiovascular Disease. Trends In Cardiovascular Medicine 1996, 6: 239-243. PMID: 21232303, DOI: 10.1016/s1050-1738(96)00091-6.Peer-Reviewed Original ResearchTissue-type plasminogen activatorFibrinolytic systemIschemic cardiovascular eventsRenin-angiotensin systemBreakdown of bradykininCardiovascular eventsAngiotensin IIT-PA secretionClinical observationsPotent stimulusStimulates releaseAngiotensin IPAI-1Plasminogen activatorVivo dataMajor inhibitorACEAngiotensinBradykininSecretionVasculature