2016
Examining EXAMINE for an Interaction With Angiotensin-Converting Enzyme Inhibition
Wilson JR, Brown NJ. Examining EXAMINE for an Interaction With Angiotensin-Converting Enzyme Inhibition. Hypertension 2016, 68: 549-551. PMID: 27480841, PMCID: PMC4982800, DOI: 10.1161/hypertensionaha.116.07884.Peer-Reviewed Original Research
2014
Substance P Increases Sympathetic Activity During Combined Angiotensin-Converting Enzyme and Dipeptidyl Peptidase-4 Inhibition
Devin JK, Pretorius M, Nian H, Yu C, Billings FT, Brown NJ. Substance P Increases Sympathetic Activity During Combined Angiotensin-Converting Enzyme and Dipeptidyl Peptidase-4 Inhibition. Hypertension 2014, 63: 951-957. PMID: 24516103, PMCID: PMC3984385, DOI: 10.1161/hypertensionaha.113.02767.Peer-Reviewed Original ResearchMeSH KeywordsAdultAngiotensin-Converting Enzyme InhibitorsBlood PressureBradykininCross-Over StudiesDipeptidyl Peptidase 4Double-Blind MethodEnalaprilatEnzyme InhibitorsFemaleHeart RateHumansMaleMiddle AgedNeurotransmitter AgentsNorepinephrinePeptidyl-Dipeptidase APyrazinesSitagliptin PhosphateSubstance PSympathetic Nervous SystemTriazolesVascular ResistanceConceptsDipeptidyl peptidase-4 inhibitionPeptidase-4 inhibitionTissue plasminogen activator releaseSubstance PDipeptidyl peptidase-4Plasminogen activator releaseSympathetic activityPeptidase-4Activator releasePlacebo-controlled crossover studyDipeptidyl peptidase-4 inhibitorsType 2 diabetes mellitusIntra-arterial enalaprilatForearm vascular resistanceForearm blood flowMean arterial pressurePeptidase-4 inhibitorsAngiotensin converting enzymeSubstrates of angiotensinVascular resistanceVasodilator responseArterial pressureBrachial arteryDiabetes mellitusCrossover study
2010
Interactive Hemodynamic Effects of Dipeptidyl Peptidase-IV Inhibition and Angiotensin-Converting Enzyme Inhibition in Humans
Marney A, Kunchakarra S, Byrne L, Brown NJ. Interactive Hemodynamic Effects of Dipeptidyl Peptidase-IV Inhibition and Angiotensin-Converting Enzyme Inhibition in Humans. Hypertension 2010, 56: 728-733. PMID: 20679179, PMCID: PMC3305047, DOI: 10.1161/hypertensionaha.110.156554.Peer-Reviewed Original ResearchMeSH KeywordsAdultAldosteroneAngiotensin-Converting Enzyme InhibitorsBlood GlucoseBlood PressureDiabetes Mellitus, Type 2Dipeptidyl Peptidase 4Dose-Response Relationship, DrugDouble-Blind MethodDrug InteractionsDrug Therapy, CombinationEnalaprilFemaleHeart RateHemodynamicsHumansInsulinMaleMetabolic SyndromeMiddle AgedPeptidyl-Dipeptidase AProspective StudiesPyrazinesRenal CirculationSitagliptin PhosphateSodiumTriazolesConceptsDipeptidyl peptidase IV inhibitionACE inhibitionHypotensive responseHemodynamic effectsBlood pressureHeart rateSerum dipeptidyl peptidase IV activityAngiotensin-Converting Enzyme InhibitionAcute ACE inhibitionVasoconstrictor neuropeptide YBlood pressure responseRenal blood flowSympathetic nervous systemType 2 diabeticsCross-over fashionDipeptidyl peptidase IV inhibitorsDose-dependent effectDipeptidyl peptidase IV activityDose-dependent mannerPeptidase IV inhibitorsPeptidase IV activityMetabolic syndromeNorepinephrine concentrationsIncretin hormonesNeuropeptide Y
2008
17&bgr;-Estradiol Increases Basal but Not Bradykinin-Stimulated Release of Active t-PA in Young Postmenopausal Women
Pretorius M, van Guilder GP, Guzman RJ, Luther JM, Brown NJ. 17&bgr;-Estradiol Increases Basal but Not Bradykinin-Stimulated Release of Active t-PA in Young Postmenopausal Women. Hypertension 2008, 51: 1190-1196. PMID: 18259028, PMCID: PMC2673569, DOI: 10.1161/hypertensionaha.107.105627.Peer-Reviewed Original ResearchConceptsYounger postmenopausal womenT-PA antigenEffect of angiotensinPostmenopausal womenT-PA releaseActive t-PAT-PAAntigen releasePlasminogen activator inhibitor-1 antigenTissue-type plasminogen activator releaseNet t-PA releaseForearm blood flowPlasminogen activator releaseEnzyme inhibitionCrossover studyIntraarterial infusionBasal releaseVascular releaseTreatment periodFibrinolytic functionPlaceboBlood flowActivator releaseAngiotensinAntigen
2007
Dipeptidyl Peptidase IV in Angiotensin-Converting Enzyme Inhibitor–Associated Angioedema
Byrd JB, Touzin K, Sile S, Gainer JV, Yu C, Nadeau J, Adam A, Brown NJ. Dipeptidyl Peptidase IV in Angiotensin-Converting Enzyme Inhibitor–Associated Angioedema. Hypertension 2007, 51: 141-147. PMID: 18025295, PMCID: PMC2749928, DOI: 10.1161/hypertensionaha.107.096552.Peer-Reviewed Original ResearchConceptsEnzyme (ACE) inhibitor-associated angioedemaDipeptidyl peptidase IV activityHistory of angiotensinPeptidase IV activityControl subjectsSubstance PDipeptidyl peptidase IVEnzyme inhibitorsLife-threatening adverse effectsAngiotensin converting enzyme (ACE) inhibitorsEnzyme inhibitionAbsence of angiotensinPrevalence of smokingSera of patientsCase-control studyPeptidase IVSubstrates of angiotensinTissue edemaAssociated angioedemaAminopeptidase P activityVascular permeabilityAngioedemaAngiotensinAminopeptidase N activityAmino-terminal degradation
2005
The Kallikrein-Kinin System: Current and Future Pharmacological Targets
Moreau ME, Garbacki N, Molinaro G, Brown NJ, Marceau F, Adam A. The Kallikrein-Kinin System: Current and Future Pharmacological Targets. Journal Of Pharmacological Sciences 2005, 99: 6-38. PMID: 16177542, DOI: 10.1254/jphs.srj05001x.Peer-Reviewed Original ResearchMeSH KeywordsAngioedemaAngiotensin-Converting Enzyme InhibitorsAnimalsAprotininBradykininBradykinin B2 Receptor AntagonistsCardiovascular DiseasesComplement C1 Inactivator ProteinsComplement C1 Inhibitor ProteinHumansInflammationKallikrein-Kinin SystemKallikreinsKidney DiseasesKininsNeprilysinPeptidyl-Dipeptidase APolymorphism, GeneticPyridinesRandomized Controlled Trials as TopicReceptor, Bradykinin B1Receptor, Bradykinin B2SerpinsThiazepinesConceptsKallikrein-kinin systemMultiple pharmacological interventionsPrecursors of kininsFuture pharmacological targetsProinflammatory effectsVasoactive kininsPharmacological interventionsCardiovascular propertiesPharmacological targetsComplement pathwayKininsActive kininsPathological processesPharmacological activitiesPlasma kallikreinMetabolic cascadeImportant metabolic pathwaysMetabolic pathwaysAntiproteasesAngiotensin-Converting Enzyme Inhibition Increases Basal Vascular Tissue Plasminogen Activator Release in Women But Not in Men
Pretorius M, Luther JM, Murphey LJ, Vaughan DE, Brown NJ. Angiotensin-Converting Enzyme Inhibition Increases Basal Vascular Tissue Plasminogen Activator Release in Women But Not in Men. Arteriosclerosis Thrombosis And Vascular Biology 2005, 25: 2435-2440. PMID: 16166566, DOI: 10.1161/01.atv.0000186185.13977.94.Peer-Reviewed Original ResearchMeSH KeywordsAdultAge FactorsAngiotensin-Converting Enzyme InhibitorsBlood PressureBradykininEnalaprilatFemaleHumansLuteal PhaseMaleMethacholine ChlorideMiddle AgedNitroprussideParasympathomimeticsPeptide FragmentsPeptidyl-Dipeptidase APostmenopausePremenopauseRegional Blood FlowSex CharacteristicsTissue Plasminogen ActivatorVasodilator AgentsConceptsT-PA releaseForearm blood flowBasal t-PA releaseNet t-PA releaseTissue plasminogen activator releasePostmenopausal womenPlasminogen activator releaseOlder menPremenopausal womenMenopausal statusActivator releaseIntra-arterial enalaprilatEffect of ACEIEndogenous bradykininHormone replacementExogenous bradykininBlood flowACEIBradykininEnalaprilatWomenYoung menMenEnzyme inhibitionRelease
2002
The relationship between plasma t‐PA and PAI‐1 levels is dependent on epistatic effects of the ACE I/D and PAI‐1 4G/5G polymorphisms
Moore J, Smolkin M, Lamb J, Brown N, Vaughan D. The relationship between plasma t‐PA and PAI‐1 levels is dependent on epistatic effects of the ACE I/D and PAI‐1 4G/5G polymorphisms. Clinical Genetics 2002, 62: 53-59. PMID: 12123488, DOI: 10.1034/j.1399-0004.2002.620107.x.Peer-Reviewed Original ResearchA comparison of combinatorial partitioning and linear regression for the detection of epistatic effects of the ACE I/D and PAI‐1 4G/5G polymorphisms on plasma PAI‐1 levels
Moore J, Lamb J, Brown N, Vaughan D. A comparison of combinatorial partitioning and linear regression for the detection of epistatic effects of the ACE I/D and PAI‐1 4G/5G polymorphisms on plasma PAI‐1 levels. Clinical Genetics 2002, 62: 74-79. PMID: 12123491, DOI: 10.1034/j.1399-0004.2002.620110.x.Peer-Reviewed Original Research
2001
Preprescription Genotyping
Roden D, Brown N. Preprescription Genotyping. Circulation 2001, 103: 1608-1610. PMID: 11273984, DOI: 10.1161/01.cir.103.12.1608.Peer-Reviewed Original Research
2000
Angiotensin-Converting Enzyme Insertion/Deletion Polymorphism Modulates the Human In Vivo Metabolism of Bradykinin
Murphey L, Gainer J, Vaughan D, Brown N. Angiotensin-Converting Enzyme Insertion/Deletion Polymorphism Modulates the Human In Vivo Metabolism of Bradykinin. Circulation 2000, 102: 829-832. PMID: 10952948, DOI: 10.1161/01.cir.102.8.829.Peer-Reviewed Original ResearchConceptsPlasma ACE activityACE activityInsertion/deletion polymorphismD genotypeD alleleBK1-5ACE I/D polymorphismEnzyme insertion/deletion polymorphismAngiotensin-Converting Enzyme Insertion/Deletion PolymorphismTissue plasminogen activator releaseAngiotensin II productionDeletion polymorphismTissue ACE activityACE D alleleACE I/IPlasminogen activator releaseFmol/mLPlasma ACE levelsBradykinin metabolismBrachial arteryVenous returnCardioprotective peptideKinin concentrationsACE levelsBradykinin concentrations
1998
ACE Insertion/Deletion Genotype Affects Bradykinin Metabolism
Brown N, Blais C, Gandhi S, Adam A. ACE Insertion/Deletion Genotype Affects Bradykinin Metabolism. Journal Of Cardiovascular Pharmacology 1998, 32: 373-377. PMID: 9733349, DOI: 10.1097/00005344-199809000-00006.Peer-Reviewed Original ResearchConceptsSerum ACE activityAng IIACE activityPlasma Ang II concentrationACE insertion/deletion genotypeACE deletion alleleAng I infusionAng II concentrationsDeleterious cardiovascular effectsACE D alleleInsertion/deletion genotypeSignificant inverse relationACE deletionCardiovascular morbidityCardiovascular effectsI infusionAng IACE genotypeACE levelsACE DDBradykinin degradationAngiotensin ID alleleSynthetic bradykininDeletion allele
1996
Angiotensin converting enzyme gene polymorphism: Potential silencer motif and impact on progression in IgA nephropathy
Hunley T, Julian B, Phillips J, Summar M, Yoshida H, Horn R, Brown N, Fogo A, Ichikawa I, Kon V. Angiotensin converting enzyme gene polymorphism: Potential silencer motif and impact on progression in IgA nephropathy. Kidney International 1996, 49: 571-577. PMID: 8821846, DOI: 10.1038/ki.1996.81.Peer-Reviewed Original ResearchConceptsRenin-angiotensin systemIgA nephropathyRenal functionDD genotypeMyocardial infarctionCardiovascular diseaseACE genotype frequenciesGene polymorphismsBiopsy-proven IgA nephropathyACE I/D polymorphismAGT 235TEnzyme deletion polymorphismNormal serum creatinineRenal disease progressionACE DD genotypeEnzyme gene polymorphismGenotype frequenciesI gene polymorphismStable creatinineAngiotensin systemSerum creatinineRenal statusVentricular hypertrophyCaucasian patientsRisk factors