2022
Comparative effects of weight loss and incretin‐based therapies on vascular endothelial function, fibrinolysis and inflammation in individuals with obesity and prediabetes: A randomized controlled trial
Mashayekhi M, Beckman JA, Nian H, Garner EM, Mayfield D, Devin JK, Koethe JR, Brown JD, Cahill KN, Yu C, Silver H, Niswender K, Luther JM, Brown NJ. Comparative effects of weight loss and incretin‐based therapies on vascular endothelial function, fibrinolysis and inflammation in individuals with obesity and prediabetes: A randomized controlled trial. Diabetes Obesity And Metabolism 2022, 25: 570-580. PMID: 36306151, PMCID: PMC10306232, DOI: 10.1111/dom.14903.Peer-Reviewed Original ResearchConceptsFlow-mediated vasodilationPlasminogen activator inhibitor-1Vascular endothelial functionEndothelial functionInsulin resistanceWeight lossGlucagon-like peptide-1 receptor agonistsBaseline flow-mediated vasodilationDipeptidyl peptidase-4 inhibitor sitagliptinGLP-1R agonist liraglutideWeight loss-independent mechanismsPeptide-1 receptor agonistsBeneficial effectsEndothelial vasodilator functionGreater endothelial dysfunctionIncretin-based therapiesNormal endothelial functionChemoattractant protein-1Chemokine MCP-1Significant weight lossActivator inhibitor-1Effect of treatmentVasodilator functionUrine albuminEndothelial dysfunction
2018
The Vasculature in Prediabetes
Wasserman DH, Wang TJ, Brown NJ. The Vasculature in Prediabetes. Circulation Research 2018, 122: 1135-1150. PMID: 29650631, PMCID: PMC5901903, DOI: 10.1161/circresaha.118.311912.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin-Converting Enzyme InhibitorsAnimalsBlood VesselsCardiovascular DiseasesCombined Modality TherapyDiabetes Mellitus, Type 2Diet, ReducingDisease ProgressionEndothelium, VascularExtracellular MatrixFatty Acids, NonesterifiedFibrinolysisGlucoseHumansHyperglycemiaHypoglycemic AgentsInflammationInsulin ResistanceLife StyleMetabolic SyndromeMiceMicrocirculationMicroRNAsMuscle, SkeletalObesityPrediabetic StateRiskWeight LossConceptsFrequency of prediabetesMainstay of treatmentPrevalence of obesityConcomitant obesityEndothelial dysfunctionExtracellular matrix remodelingDiabetes mellitusEndothelial functionRenal diseaseMetabolic derangementsFibrinolytic dysfunctionEndothelial vasodilatorsInsulin resistanceInsulin sensitivityCardiovascular diseaseDelivery of insulinSlow progressionPrediabetesWeight lossSkeletal muscleMatrix remodelingMellitusObesityDysfunctionDiseaseDipeptidyl Peptidase‐4 Inhibition Potentiates Stimulated Growth Hormone Secretion and Vasodilation in Women
Wilson JR, Brown NJ, Nian H, Yu C, Bidlingmaier M, Devin JK. Dipeptidyl Peptidase‐4 Inhibition Potentiates Stimulated Growth Hormone Secretion and Vasodilation in Women. Journal Of The American Heart Association 2018, 7: e008000. PMID: 29478970, PMCID: PMC5866333, DOI: 10.1161/jaha.117.008000.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, OralAdultCross-Over StudiesDipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsDouble-Blind MethodFemaleFibrinolysisHuman Growth HormoneHumansInsulin-Like Growth Factor IMaleSecretory PathwaySex FactorsSitagliptin PhosphateTime FactorsTissue Plasminogen ActivatorUp-RegulationVasodilationYoung AdultConceptsFree insulin-like growth factor-1Insulin-like growth factor-1Growth factor-1GH secretionGrowth hormoneGHR blockadeVascular resistanceFactor 1Nitric oxideTissue plasminogen activator activityPeptidase-4 inhibitionImpaired endothelial functionGrowth hormone secretionReceptor-dependent effectsDipeptidyl peptidase-4Study drugEndothelial functionPlasminogen activator activityCrossover studyHormone secretionPeptidase-4VasodilationHealthy adultsGH receptorInhibition potentiates
2015
Treatment with Sildenafil Improves Insulin Sensitivity in Prediabetes: A Randomized, Controlled Trial
Ramirez CE, Nian H, Yu C, Gamboa JL, Luther JM, Brown NJ, Shibao CA. Treatment with Sildenafil Improves Insulin Sensitivity in Prediabetes: A Randomized, Controlled Trial. The Journal Of Clinical Endocrinology & Metabolism 2015, 100: 4533-4540. PMID: 26580240, PMCID: PMC4667163, DOI: 10.1210/jc.2015-3415.Peer-Reviewed Original ResearchMeSH KeywordsAdultAlbuminuriaDouble-Blind MethodEndothelium, VascularFemaleFibrinolysisGlucoseGlucose Clamp TechniqueGlucose Tolerance TestHemodynamicsHumansInsulinInsulin ResistanceMaleMiddle AgedOverweightPhosphodiesterase 5 InhibitorsPlasminogen Activator Inhibitor 1Prediabetic StateSildenafil CitrateConceptsPhosphodiesterase-5 inhibitionGlucose-stimulated insulin secretionInsulin sensitivity indexInsulin sensitivityInsulin secretionBaseline insulin sensitivity indexPlacebo-controlled studyClinical Research CenterBody mass indexEnd of treatmentPlasminogen activator inhibitor-1Tissue plasminogen activatorActivator inhibitor-1Placebo groupUrine albuminSildenafil groupCreatinine ratioEndothelial functionPrimary outcomeMass indexTreatment armsFibrinolytic balanceDisposition indexHyperglycemic clampOverweight individuals
2012
Contribution of Endogenous Bradykinin to Fibrinolysis, Inflammation, and Blood Product Transfusion Following Cardiac Surgery: A Randomized Clinical Trial
Balaguer JM, Yu C, Byrne JG, Ball SK, Petracek MR, Brown NJ, Pretorius M. Contribution of Endogenous Bradykinin to Fibrinolysis, Inflammation, and Blood Product Transfusion Following Cardiac Surgery: A Randomized Clinical Trial. Clinical Pharmacology & Therapeutics 2012, 93: 326-334. PMID: 23361105, PMCID: PMC4031681, DOI: 10.1038/clpt.2012.249.Peer-Reviewed Original ResearchConceptsBradykinin B2 receptor antagonismB2 receptor antagonismCardiopulmonary bypassEndogenous bradykininTissue-type plasminogen activatorHoe 140Receptor antagonismBradykinin B2 receptor antagonistSubsequent transfusion requirementsBlood product transfusionProportion of patientsB2 receptor antagonistD-dimer concentrationD-dimer formationEACA treatmentTransfusion requirementsPostoperative bleedingProduct transfusionBlood lossCardiac surgeryInflammatory cytokinesReceptor antagonistClinical trialsFibrinolytic capacityInflammatory responseComparative Effects of Angiotensin Receptor Blockade and ACE Inhibition on the Fibrinolytic and Inflammatory Responses to Cardiopulmonary Bypass
Billings F, Balaguer J, Yu C, Wright P, Petracek M, Byrne J, Brown N, Pretorius M. Comparative Effects of Angiotensin Receptor Blockade and ACE Inhibition on the Fibrinolytic and Inflammatory Responses to Cardiopulmonary Bypass. Clinical Pharmacology & Therapeutics 2012, 91: 1065-1073. PMID: 22549281, PMCID: PMC3822756, DOI: 10.1038/clpt.2011.356.Peer-Reviewed Original ResearchMeSH KeywordsAgedAngiotensin II Type 1 Receptor BlockersAngiotensin-Converting Enzyme InhibitorsBenzimidazolesBiphenyl CompoundsBlood TransfusionBradykininCardiopulmonary BypassEndpoint DeterminationFemaleFibrinolysisHematocritHospital MortalityHumansInflammationInterleukinsLength of StayMaleMiddle AgedMonitoring, IntraoperativePerioperative CarePostoperative ComplicationsRamiprilTetrazolesTreatment OutcomeConceptsAngiotensin II type 1 receptor blockadeACE inhibitionCardiopulmonary bypassReceptor blockadeInflammatory responseType 1 receptor blockadeTissue-type plasminogen activator concentrationAngiotensin receptor blockadeEffect of angiotensinRed cell transfusionDay of surgeryPlasminogen activator inhibitor-1Activator inhibitor-1Plasminogen activator concentrationsHospital stayPlasma transfusionIL-10ACE inhibitorsIL-8Intraoperative fibrinolysisFibrinolysisInhibitor-1Comparative effectsPlaceboTransfusion
2010
Review: Therapeutic potential of plasminogen activator inhibitor-1 inhibitors
Brown NJ. Review: Therapeutic potential of plasminogen activator inhibitor-1 inhibitors. Therapeutic Advances In Cardiovascular Disease 2010, 4: 315-324. PMID: 20660535, DOI: 10.1177/1753944710379126.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1Plasminogen Activator Inhibitor-1 InhibitorsInitiation of diabetesPathogenesis of thrombosisPotential therapeutic strategyActivator inhibitor-1Major physiological inhibitorRenal injuryVascular remodelingPreclinical studiesTherapeutic strategiesSmall molecule inhibitorsTherapeutic potentialInhibitor-1Physiological inhibitorMolecule inhibitorsCell migrationInhibitorsThrombosisDiabetesFibrosisPathogenesisFibrinolysisInjuryDisease
2009
Endogenous Bradykinin Contributes to Increased Plasminogen Activator Inhibitor 1 Antigen following Hemodialysis
Marney AM, Ma J, Luther JM, Ikizler TA, Brown NJ. Endogenous Bradykinin Contributes to Increased Plasminogen Activator Inhibitor 1 Antigen following Hemodialysis. Journal Of The American Society Of Nephrology 2009, 20: 2246-2252. PMID: 19628666, PMCID: PMC2754101, DOI: 10.1681/asn.2009050505.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1 antigenHoe 140Endogenous bradykininHemodialysis patientsMCP-1Receptor blocker HOE-140Placebo-controlled crossover studyOxidative stressChronic hemodialysis patientsMean arterial pressureCoronary artery diseaseKallikrein-kinin systemBradykinin receptor antagonismHeart rate responsePAI-1 antigenTissue plasminogen activatorEffect of dialysisEnd of dialysisProduction of bradykininInhibits platelet aggregationCardiovascular eventsHemodialysis populationArterial pressureArtery diseaseEndothelial release
2008
Male–female differences in the genetic regulation of t-PA and PAI-1 levels in a Ghanaian population
Schoenhard JA, Asselbergs FW, Poku KA, Stocki SA, Gordon S, Vaughan DE, Brown NJ, Moore JH, Williams SM. Male–female differences in the genetic regulation of t-PA and PAI-1 levels in a Ghanaian population. Human Genetics 2008, 124: 479-488. PMID: 18953568, PMCID: PMC2770717, DOI: 10.1007/s00439-008-0573-x.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1PAI-1 levelsTissue-type plasminogen activatorRenin polymorphismPAI-1 4G/5G polymorphismRenin-angiotensin systemDiastolic blood pressurePopulation-based sampleActivator inhibitor-1Large-scale population-based samplePAI-1 expressionBlood pressureTotal cholesterolThromboembolic diseasePlasma levelsRisk factorsCardiovascular diseaseD polymorphismMetabolic parametersG polymorphismFibrinolytic systemGene polymorphismsThrombus formationCaucasian subjectsGhanaian population
2006
Bradykinin and Its Metabolite Bradykinin 1-5 Inhibit Thrombin-Induced Platelet Aggregation in Humans
Murphey LJ, Malave HA, Petro J, Biaggioni I, Byrne DW, Vaughan DE, Luther JM, Pretorius M, Brown NJ. Bradykinin and Its Metabolite Bradykinin 1-5 Inhibit Thrombin-Induced Platelet Aggregation in Humans. Journal Of Pharmacology And Experimental Therapeutics 2006, 318: 1287-1292. PMID: 16772538, DOI: 10.1124/jpet.106.104026.Peer-Reviewed Original ResearchConceptsForearm blood flowNet t-PA releaseT-PA releaseThrombin-induced platelet aggregationPlatelet aggregationBradykinin 1Thrombin receptor-activating peptide-induced platelet aggregationTissue plasminogen activator antigenMajor stable metabolitePeptide-induced platelet aggregationDoses of bradykininThrombin receptor-activating peptideAntecubital venous bloodPlasminogen activator antigenArterial plasma samplesDose-dependent increaseGamma-thrombinReceptor-activating peptidePlatelet-rich plasmaPmol/minPeptide infusionBrachial arteryVenous bloodHealthy subjectsBlood flowEndogenous NO Regulates Plasminogen Activator Inhibitor-1 During Angiotensin-Converting Enzyme Inhibition
Brown NJ, Muldowney JA, Vaughan DE. Endogenous NO Regulates Plasminogen Activator Inhibitor-1 During Angiotensin-Converting Enzyme Inhibition. Hypertension 2006, 47: 441-448. PMID: 16432054, DOI: 10.1161/01.hyp.0000202478.79587.1a.Peer-Reviewed Original ResearchMeSH KeywordsAdultAldosteroneAngiotensin-Converting Enzyme InhibitorsArginineDouble-Blind MethodDrug CombinationsEnzyme InhibitorsFemaleFibrinolysisHemodynamicsHumansInfusions, IntravenousMaleMiddle AgedNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthasePlasminogen Activator Inhibitor 1ProdrugsRamiprilReference ValuesRenin-Angiotensin SystemConceptsPlasminogen activator inhibitor-1Plasminogen activator inhibitor-1 antigenActivator inhibitor-1Salt-replete subjectsL-arginineFibrinolytic balanceInhibitor-1Angiotensin-Converting Enzyme InhibitionNO precursor L-argininePlasminogen activator inhibitor antigenTissue-type plasminogen activator antigenEffect of angiotensinPrecursor L-argininePlasminogen activator antigenNO synthase inhibitorEnzyme inhibitionT-PA activityRenin activityD-dimerInhibitor antigenNormal subjectsSynthase inhibitorEnzyme inhibitorsT-PAAntigen
2005
A pilot study indicating that bradykinin B2 receptor antagonism attenuates protamine‐related hypotension after cardiopulmonary bypass
Pretorius M, Scholl FG, McFarlane JA, Murphey LJ, Brown NJ. A pilot study indicating that bradykinin B2 receptor antagonism attenuates protamine‐related hypotension after cardiopulmonary bypass. Clinical Pharmacology & Therapeutics 2005, 78: 477-485. PMID: 16321614, DOI: 10.1016/j.clpt.2005.08.010.Peer-Reviewed Original ResearchConceptsMean arterial pressureSaline solution groupT-PA activityAdministration of protamineCardiopulmonary bypassProtamine administrationHoe 140Receptor antagonismBradykinin concentrationsSolution groupTissue-type plasminogen activator releaseACE inhibitor-treated patientsBradykinin B2 receptor antagonismReceptor antagonist HOE 140Angiotensin-converting enzyme inhibitorB2 receptor antagonismInhibitor-treated patientsElective cardiac surgeryAdult male patientsBradykinin receptor antagonismDegradation of bradykininPlasminogen activator releaseSaline solutionProtamine infusionArterial pressureMelanocortin-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
2004
Angiotensin‐converting enzyme inhibition and smoking potentiate the kinin response to cardiopulmonary bypass
Pretorius M, McFarlane JA, Vaughan DE, Brown NJ, Murphey LJ. Angiotensin‐converting enzyme inhibition and smoking potentiate the kinin response to cardiopulmonary bypass. Clinical Pharmacology & Therapeutics 2004, 76: 379-387. PMID: 15470338, DOI: 10.1016/j.clpt.2004.06.004.Peer-Reviewed Original ResearchConceptsACE inhibitor groupMinutes of CPBCardiopulmonary bypassACE inhibitorsInhibitor groupKinin responseBradykinin concentrationsEffects of CPBCoronary artery bypass surgeryTissue-type plasminogen activator antigenPreoperative ACE inhibitorsArtery bypass surgeryPostoperative day 1Concentrations of bradykininEffect of smokingPlasminogen activator antigenKallikrein-kinin systemSignificant inverse correlationArterial pressureBypass surgeryFibrinolytic responseVenous bloodACE activityDay 1Enzyme inhibitors
2003
Angiotensin-Converting Enzyme Inhibition Alters the Fibrinolytic Response to Cardiopulmonary Bypass
Pretorius M, Murphey LJ, McFarlane JA, Vaughan DE, Brown NJ. Angiotensin-Converting Enzyme Inhibition Alters the Fibrinolytic Response to Cardiopulmonary Bypass. Circulation 2003, 108: 3079-3083. PMID: 14656921, DOI: 10.1161/01.cir.0000105765.54573.60.Peer-Reviewed Original ResearchConceptsPostoperative day 1PAI-1 antigenCardiopulmonary bypassACE inhibitorsPAI-1 expressionACEI groupACE inhibitionPlasminogen activator inhibitor-1 (PAI-1) concentrationsTPA activityTissue-type plasminogen activator antigenAngiotensin-converting enzyme inhibitionAcute graft thrombosisPreoperative ACE inhibitorsMorning of surgeryCoronary artery bypassVein graft occlusionPlasminogen activator antigenArterial blood samplesArtery bypassGraft thrombosisGraft occlusionFibrinolytic responseAngiotensin IIBlood samplesDay 1Effect of Combined AT1 Receptor and Aldosterone Receptor Antagonism on Plasminogen Activator Inhibitor-1
Sawathiparnich P, Murphey LJ, Kumar S, Vaughan DE, Brown NJ. Effect of Combined AT1 Receptor and Aldosterone Receptor Antagonism on Plasminogen Activator Inhibitor-1. The Journal Of Clinical Endocrinology & Metabolism 2003, 88: 3867-3873. PMID: 12915681, DOI: 10.1210/jc.2003-030374.Peer-Reviewed Original ResearchMeSH KeywordsAdultAngiotensin Receptor AntagonistsBenzimidazolesBiphenyl CompoundsDiureticsElectrolytesFemaleFibrinolysisFurosemideHemodynamicsHumansMaleMineralocorticoid Receptor AntagonistsPlasminogen Activator Inhibitor 1Potassium ChlorideReceptor, Angiotensin, Type 1Renin-Angiotensin SystemSingle-Blind MethodSpironolactoneTetrazolesConceptsMean arterial pressureAldosterone receptor antagonismAng IIReceptor antagonismPAI-1Angiotensin II type 1Coadministration of spironolactoneEffects of candesartanFurosemide-induced increasePresence of candesartanAldosterone receptor antagonistsEndogenous Ang IIPlasminogen activator inhibitor-1PAI-1 antigenActivator inhibitor-1PAI-1 productionPlasminogen activator inhibitorAldosterone systemNormotensive subjectsArterial pressureAngiotensin IIAT1 receptorFibrinolytic variablesReceptor antagonistCandesartanAngiotensin-Converting Enzyme Inhibition Increases Human Vascular Tissue-Type Plasminogen Activator Release Through Endogenous Bradykinin
Pretorius M, Rosenbaum D, Vaughan DE, Brown NJ. Angiotensin-Converting Enzyme Inhibition Increases Human Vascular Tissue-Type Plasminogen Activator Release Through Endogenous Bradykinin. Circulation 2003, 107: 579-585. PMID: 12566370, DOI: 10.1161/01.cir.0000046268.59922.a4.Peer-Reviewed Original ResearchMeSH KeywordsAdultAngiotensin-Converting Enzyme InhibitorsBlood Flow VelocityBradykininBradykinin Receptor AntagonistsDose-Response Relationship, DrugEnalaprilatEndothelium, VascularFemaleFibrinolysisForearmHumansInfusions, Intra-ArterialMaleMethacholine ChlorideMuscarinic AgonistsRegional Blood FlowSmokingTissue Plasminogen ActivatorVascular ResistanceConceptsForearm blood flowNet t-PA releaseT-PA releaseEndothelial t-PA releaseHoe 140T-PA responseEndogenous bradykininACE inhibitionExogenous bradykininTissue-type plasminogen activator releaseReceptor antagonist HOE 140Angiotensin-Converting Enzyme InhibitionBradykinin receptor antagonist HOE 140Effects of enalaprilatIntra-arterial enalaprilatIntra-arterial infusionPlasminogen activator releaseEnzyme inhibitionFBF responseVascular resistanceBlood flowActivator releaseEnalaprilatBradykininMethacholine
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 ResearchMeSH KeywordsDisease ProgressionFibrinolysisHumansKidney DiseasesPlasminogen Activator Inhibitor 1Renin-Angiotensin SystemConceptsPlasminogen 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 pathwayDiseaseInjuryRAASSpironolactone Abolishes the Relationship between Aldosterone and Plasminogen Activator Inhibitor-1 in Humans
Sawathiparnich P, Kumar S, Vaughan DE, Brown NJ. Spironolactone Abolishes the Relationship between Aldosterone and Plasminogen Activator Inhibitor-1 in Humans. The Journal Of Clinical Endocrinology & Metabolism 2002, 87: 448-452. PMID: 11836266, DOI: 10.1210/jcem.87.2.7980.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAldosteroneAntihypertensive AgentsBlood PressureCross-Over StudiesDiureticsDouble-Blind MethodFibrinolysisHumansHydrochlorothiazideHypertensionMaleMiddle AgedMineralocorticoid Receptor AntagonistsPlasminogen Activator Inhibitor 1Sodium Chloride Symporter InhibitorsSpironolactoneConceptsPAI-1 antigenT-PA antigenAngiotensin IITissue-type plasminogen activator antigenEffect of spironolactoneSystolic blood pressureMale hypertensive subjectsPlasminogen activator antigenPlasminogen activator inhibitor-1Plasminogen activator inhibitor-1 productionActivator inhibitor-1PAI-1 productionAldosterone systemHypertensive subjectsSerum aldosteroneBlood pressureEndogenous aldosteroneHemodynamic parametersAldosteroneStudy daysSpironolactoneHCTZPAI-1AntigenInhibitor-1
2001
Interactive Effect of PAI-1 4G/5G Genotype and Salt Intake on PAI-1 Antigen
Brown N, Murphey L, Srikuma N, Koschachuhanan N, Williams G, Vaughan D. Interactive Effect of PAI-1 4G/5G Genotype and Salt Intake on PAI-1 Antigen. Arteriosclerosis Thrombosis And Vascular Biology 2001, 21: 1071-1077. PMID: 11397722, DOI: 10.1161/01.atv.21.6.1071.Peer-Reviewed Original ResearchConceptsPAI-1 4G/5G genotypePAI-1 antigen concentrationsPAI-1 antigenHigh salt intakeLow salt intakeSalt intakeG genotypeAntigen concentrationThrombotic cardiovascular eventsPlasma renin activityPAI-1 expressionPAI-1 geneAldosterone systemCardiovascular eventsCardiovascular morbidityRenin activityPharmacological therapyEssential hypertensionSerum triglyceridesEffects of activationG polymorphismG homozygotesG groupAntigenIntake