2024
TRPV1 corneal neuralgia mutation: Enhanced pH response, bradykinin sensitization, and capsaicin desensitization
Gualdani R, Barbeau S, Yuan J, Jacobs D, Gailly P, Dib-Hajj S, Waxman S. TRPV1 corneal neuralgia mutation: Enhanced pH response, bradykinin sensitization, and capsaicin desensitization. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2406186121. PMID: 39226353, PMCID: PMC11406256, DOI: 10.1073/pnas.2406186121.Peer-Reviewed Original ResearchConceptsLaser-assisted in situ keratomileusisPhotorefractive keratectomyOcular Surface Disease Index scoreCapsaicin-induced desensitizationPhotorefractive keratectomy enhancementDisease Index scorePhysiological membrane potentialsCorneal neuralgiaTRPV1 variantsCorneal painRefractive surgeryRefractive errorCapsaicin desensitizationPersistent painBradykinin sensitivityNerve injuryM mutationPatch clampChannel activitySurgical techniqueLeftward shiftInflammatory mediatorsM-channelPainIndex score
2023
Bradykinin B2 receptor blockade and intradialytic hypotension
Gamboa J, Mambungu C, Clagett A, Nian H, Yu C, Ikizler T, Brown N. Bradykinin B2 receptor blockade and intradialytic hypotension. BMC Nephrology 2023, 24: 134. PMID: 37170244, PMCID: PMC10176680, DOI: 10.1186/s12882-023-03192-4.Peer-Reviewed Original ResearchConceptsBradykinin B2 receptor blockadeB2 receptor blockadeMaintenance hemodialysisBlood pressureReceptor blockersReceptor blockadeIntradialytic hypotensionBradykinin B2 receptor blockerLack of vasoconstrictionProduction of vasodilatorsSystolic blood pressureGroup of patientsCrossover clinical trialCommon clinical complicationHemodynamic effectsClinical complicationsContinuous infusionClinical trialsStratified analysisIcatibantHemodialysisPatientsHypotensionPlaceboCompensatory mechanisms
2021
Immunomodifying and neuroprotective effects of noscapine: Implications for multiple sclerosis, neurodegenerative, and psychiatric disorders
Altinoz M, Guloksuz S, Ozpinar A. Immunomodifying and neuroprotective effects of noscapine: Implications for multiple sclerosis, neurodegenerative, and psychiatric disorders. Chemico-Biological Interactions 2021, 352: 109794. PMID: 34963564, DOI: 10.1016/j.cbi.2021.109794.Peer-Reviewed Original ResearchMeSH KeywordsAlzheimer DiseaseAmyotrophic Lateral SclerosisAnimalsBradykininHistamine AntagonistsHumansImmunomodulating AgentsIon ChannelsMental DisordersMultiple SclerosisNeurodegenerative DiseasesNeuroprotective AgentsNoscapineOligodendrogliaParkinsonian DisordersReceptors, G-Protein-CoupledSignal TransductionStrokeConceptsNeuroprotective effectsMultiple sclerosisInflammatory transcription factor NF-κBIschemic brain damageNeonatal rat pupsPilot clinical studyAmyotrophic lateral sclerosisTranscription factor NF-κBCortical neuronal cellsSignificant therapeutic efficacyFactor NF-κBBitter taste receptorsHistaminergic systemBrain damageRat pupsClinical studiesSK channelsLateral sclerosisParkinson's diseaseAnxiolytic activityPsychiatric disordersChemical injuryNF-κBAnimal modelsPsychiatric diseases
2020
A mechanistic model and therapeutic interventions for COVID-19 involving a RAS-mediated bradykinin storm
Garvin M, Alvarez C, Miller JI, Prates ET, Walker AM, Amos BK, Mast AE, Justice A, Aronow B, Jacobson D. A mechanistic model and therapeutic interventions for COVID-19 involving a RAS-mediated bradykinin storm. ELife 2020, 9: e59177. PMID: 32633718, PMCID: PMC7410499, DOI: 10.7554/elife.59177.Peer-Reviewed Original ResearchConceptsBronchoalveolar lavage fluidCOVID-19COVID-19 patientsBradykinin stormRAS receptorsLavage fluidVasopressor systemsBradykinin levelsVascular dilationVascular permeabilityBradykinin receptorsTherapeutic interventionsTherapeutic intervention pointNovel molecular mechanismDecreased expressionACE2Atypical patternsDisease mechanismsHypotensionAngiotensinMultiple tissuesCritical imbalanceReceptorsMolecular mechanismsVirus
2018
Bradykinin B2 Receptor Contributes to Inflammatory Responses in Human Endothelial Cells by the Transactivation of the Fibroblast Growth Factor Receptor FGFR-1
Terzuoli E, Corti F, Nannelli G, Giachetti A, Donnini S, Ziche M. Bradykinin B2 Receptor Contributes to Inflammatory Responses in Human Endothelial Cells by the Transactivation of the Fibroblast Growth Factor Receptor FGFR-1. International Journal Of Molecular Sciences 2018, 19: 2638. PMID: 30200598, PMCID: PMC6163484, DOI: 10.3390/ijms19092638.Peer-Reviewed Original ResearchConceptsFibroblast growth factor receptor 1Human umbilical vein endothelial cellsCell permeabilityEndothelial cellsFGFR-1 phosphorylationEndothelial cell permeabilityFGF-2 signalingFGF-2 pathwaysFGF-2/FGFRFGFR-1 inhibitorsC-SrcGrowth factor receptor 1Umbilical vein endothelial cellsDownstream signalingHuman endothelial cellsGrowth factor 2Vein endothelial cellsFactor receptor 1Cell migrationFGF-2 upregulationAmplification loopSignalingFactor 2Angiogenic disordersBradykinin B2 receptorEndogenous bradykinin and B1-B5 during angiotensin-converting enzyme inhibitor–associated angioedema
Hubers S, Kohm K, Wei S, Yu C, Nian H, Grabert R, Sexton DJ, Brown NJ. Endogenous bradykinin and B1-B5 during angiotensin-converting enzyme inhibitor–associated angioedema. Journal Of Allergy And Clinical Immunology 2018, 142: 1636-1639.e5. PMID: 30036596, PMCID: PMC6226317, DOI: 10.1016/j.jaci.2018.06.037.Peer-Reviewed Original Research
2017
Angiotensin-converting Enzyme Inhibitor and Other Drug-associated Angioedema
Stone C, Brown NJ. Angiotensin-converting Enzyme Inhibitor and Other Drug-associated Angioedema. Immunology And Allergy Clinics Of North America 2017, 37: 483-495. PMID: 28687104, DOI: 10.1016/j.iac.2017.04.006.Peer-Reviewed Original ResearchConceptsDrug-induced angioedemaEnzyme inhibitorsAngiotensin-converting enzyme inhibitorNon-β-lactam antibioticsNonsteroidal antiinflammatory agentsNonallergic angioedemaSubstance PTherapeutic decisionsAngioedemaAntiinflammatory agentsLactam antibioticsOther DrugΒ-lactam antibioticsDrugsPatientsLeukotrienesBradykininGenetic variantsAntibioticsInhibitorsAngiotensinProstaglandinsAgentsHistamineMainstay
2016
Effect of bradykinin receptor antagonism on ACE inhibitor-associated angioedema
Straka BT, Ramirez CE, Byrd JB, Stone E, Woodard-Grice A, Nian H, Yu C, Banerji A, Brown NJ. Effect of bradykinin receptor antagonism on ACE inhibitor-associated angioedema. Journal Of Allergy And Clinical Immunology 2016, 140: 242-248.e2. PMID: 27913306, PMCID: PMC5705179, DOI: 10.1016/j.jaci.2016.09.051.Peer-Reviewed Original ResearchConceptsACE inhibitor-associated angioedemaResolution of symptomsVisual analog scaleAnalog scaleReceptor antagonistTreatment groupsBradykinin BEnzyme (ACE) inhibitor-associated angioedemaStudy drug administrationReceptor antagonist icatibantHours of presentationTreatment of attacksC1 inhibitor deficiencyBradykinin receptor antagonismFrequency of administrationVanderbilt University Medical CenterUniversity Medical CenterMassachusetts General HospitalTwo-thirdsAntagonist icatibantBowel edemaWhite patientsH2 blockersClinical efficacyInhibitor deficiencyTwo functionally distinct pools of eNOS in endothelium are facilitated by myoendothelial junction lipid composition
Biwer L, Taddeo E, Kenwood B, Hoehn K, Straub A, Isakson B. Two functionally distinct pools of eNOS in endothelium are facilitated by myoendothelial junction lipid composition. Biochimica Et Biophysica Acta 2016, 1861: 671-679. PMID: 27106139, PMCID: PMC4869716, DOI: 10.1016/j.bbalip.2016.04.014.Peer-Reviewed Original ResearchMeSH KeywordsBiological TransportBradykininCalciumCalcium SignalingCell CommunicationCoculture TechniquesCyclic GMPDiglyceridesEgtazic AcidEndoplasmic ReticulumEndothelial CellsGap JunctionsGene Expression RegulationHumansInositol 1,4,5-TrisphosphateMacrocyclic CompoundsMyocytes, Smooth MuscleNitric Oxide Synthase Type IIIOxazolesPhenylephrinePhosphatidylserinesPhosphorylationPrimary Cell CultureProtein Kinase CProtein Kinase InhibitorsThapsigarginCombined Angiotensin Receptor Antagonism and Neprilysin Inhibition
Hubers SA, Brown NJ. Combined Angiotensin Receptor Antagonism and Neprilysin Inhibition. Circulation 2016, 133: 1115-1124. PMID: 26976916, PMCID: PMC4800749, DOI: 10.1161/circulationaha.115.018622.Peer-Reviewed Original ResearchMeSH KeywordsAbnormalities, Drug-InducedAminobutyratesAngioedemaAngiotensin Receptor AntagonistsBiphenyl CompoundsBradykininContraindicationsDrug CombinationsDrug CostsDrug SynergismEnalaprilEnzyme InhibitorsFemaleFollow-Up StudiesHeart FailureHumansHyperkalemiaHypertensionKidneyMulticenter Studies as TopicNatriuretic PeptidesNeprilysinPregnancyProdrugsProspective StudiesPyridinesRandomized Controlled Trials as TopicStroke VolumeTetrazolesThiazepinesValsartanConceptsValsartan/sacubitrilReduced ejection fractionHeart failureNatriuretic peptideEjection fractionN-terminal pro-brain natriuretic peptideNeprilysin inhibitor prodrug sacubitrilPro-brain natriuretic peptideAngiotensin receptor blocker valsartanAngiotensin receptor antagonismAngiotensin receptor blockersHeart Failure TrialReceptor blocker valsartanAngiotensin receptor antagonistsBrain natriuretic peptideOngoing clinical trialsMechanism of actionNeprilysin inhibitionAldosterone antagonistsAldosterone systemReceptor blockersBlood pressureFailure TrialPathophysiological mechanismsReceptor antagonism
2015
Angiotensin converting enzyme inhibition increases ADMA concentration in patients on maintenance hemodialysis – a randomized cross-over study
Gamboa JL, Pretorius M, Sprinkel KC, Brown NJ, Ikizler TA. Angiotensin converting enzyme inhibition increases ADMA concentration in patients on maintenance hemodialysis – a randomized cross-over study. BMC Nephrology 2015, 16: 167. PMID: 26494370, PMCID: PMC4618919, DOI: 10.1186/s12882-015-0162-x.Peer-Reviewed Original ResearchConceptsEnd-stage renal diseaseAngiotensin receptor blockersMaintenance hemodialysisCross-over studyADMA levelsAsymmetric dimethylarginineACE inhibitionADMA productionADMA concentrationsShort-term ACE inhibitionRandomized cross-over studyIntracellular ADMA concentrationStudy of patientsEffect of bradykininB2 receptor stimulationACE inhibitor-induced increaseInhibitor-induced increaseRamipril treatmentCardiovascular morbidityReceptor blockersEndothelial dysfunctionRenal diseaseBradykinin levelsBackgroundEndothelial dysfunctionDialysis session
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
2013
The Development of a Novel Molecular Assay Examining the Role of Aminopeptidase P Polymorphisms in Acute Hypotensive Transfusion Reactions
Hui Y, Wu Y, Tormey CA. The Development of a Novel Molecular Assay Examining the Role of Aminopeptidase P Polymorphisms in Acute Hypotensive Transfusion Reactions. Archives Of Pathology & Laboratory Medicine 2013, 137: 96-9. PMID: 23276181, DOI: 10.5858/arpa.2011-0466-oa.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAdolescentAgedAminopeptidasesAngiotensin-Converting Enzyme InhibitorsBase SequenceBradykininCase-Control StudiesDNA PrimersFemaleGenetic Predisposition to DiseaseHeterozygoteHomozygoteHumansHypotensionMaleMiddle AgedPolymerase Chain ReactionPolymorphism, Single NucleotideTransfusion ReactionConceptsAcute hypotensive transfusion reactionsHypotensive transfusion reactionsACE-IsTransfusion reactionsSingle nucleotide polymorphismsMolecular assaysHarmful adverse effectsPolymerase chain reactionBradykinin degradationPatientsEnzyme inhibitorsBradykinin generationAPP geneNovel molecular assayPilot studyAdverse effectsChain reactionFurther studiesAminopeptidase PXPNPEP2PolymorphismAssaysAPP activitySequencing resultsTransfusion
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 responsePolymorphisms in the transcription factor NRF2 and forearm vasodilator responses in humans
Marczak ED, Marzec J, Zeldin DC, Kleeberger SR, Brown NJ, Pretorius M, Lee CR. Polymorphisms in the transcription factor NRF2 and forearm vasodilator responses in humans. Pharmacogenetics And Genomics 2012, 22: 620-628. PMID: 22668754, PMCID: PMC3599320, DOI: 10.1097/fpc.0b013e32835516e5.Peer-Reviewed Original ResearchConceptsForearm vascular resistanceForearm blood flowVariant allele carriersVasodilator responseSodium nitroprussideVascular functionAllele carriersStrain-gauge venous occlusion plethysmographyLower forearm blood flowEndothelial-independent mannerForearm vasodilator responseVenous occlusion plethysmographyWild-type individualsTranscription factor Nrf2Endothelial dysfunctionOcclusion plethysmographyVascular resistanceIncremental dosesCardiovascular diseaseBlood flowG genotypeA polymorphismSignificant associationBasal conditionsFactor Nrf2Comparative 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
Genetic Variation in Soluble Epoxide Hydrolase (EPHX2) Is Associated With Forearm Vasodilator Responses in Humans
Lee CR, Pretorius M, Schuck RN, Burch LH, Bartlett J, Williams SM, Zeldin DC, Brown NJ. Genetic Variation in Soluble Epoxide Hydrolase (EPHX2) Is Associated With Forearm Vasodilator Responses in Humans. Hypertension 2010, 57: 116-122. PMID: 21098312, PMCID: PMC3020911, DOI: 10.1161/hypertensionaha.110.161695.Peer-Reviewed Original ResearchConceptsForearm blood flowVariant allele carriersForearm vasodilator responseForearm vascular resistanceSoluble epoxide hydrolaseVascular resistanceVasodilator responseBlood flowAllele carriersSodium nitroprussideVascular functionStrain-gauge venous occlusion plethysmographyHighest forearm blood flowLower forearm vascular resistanceSignificant associationCytochrome P450-derived epoxyeicosatrienoic acidsEpoxide hydrolaseVenous occlusion plethysmographyCardiovascular disease riskEndothelium-independent mannerWild-type individualsOcclusion plethysmographyPotent vasodilatorEpoxyeicosatrienoic acidsPreclinical modelsBradykinin forming capacity of oversulfated chondroitin sulfate contaminated heparin in vitro
Adam A, Montpas N, Keire D, Désormeaux A, Brown NJ, Marceau F, Westenberger B. Bradykinin forming capacity of oversulfated chondroitin sulfate contaminated heparin in vitro. Biomaterials 2010, 31: 5741-5748. PMID: 20427081, PMCID: PMC2896062, DOI: 10.1016/j.biomaterials.2010.03.074.Peer-Reviewed Original ResearchConceptsContact system activationAnaphylactoid reactionsOversulfated chondroitin sulfateSystem activationSevere anaphylactoid reactionPlasma contact systemHuman plasmaInflammatory peptidesChondroitin sulfateEnzyme inhibitorsBK releaseDrug AdministrationBradykininHeparinSignificant correlationDefinitive evidenceDextran sulfatePlasma dilutionActivationConclusionPatientsPathophysiologyKininsAdministrationPlasmaIncreased blood flow induces oxidative stress through an endothelium- and nitric oxide-independent mechanism
Fong P, Stafforini DM, Brown NJ, Pretorius M. Increased blood flow induces oxidative stress through an endothelium- and nitric oxide-independent mechanism. Free Radical Biology And Medicine 2010, 49: 301-305. PMID: 20423727, PMCID: PMC2916026, DOI: 10.1016/j.freeradbiomed.2010.04.023.Peer-Reviewed Original ResearchConceptsForearm blood flowHypertensive subjectsL-NMMAIsoprostane releaseBlood flowOxidative stressBasal forearm blood flowNitric oxide-independent mechanismEndothelium-independent mechanismNO synthase inhibitorEffect of bradykininMonomethyl-L-arginineIntraarterial bradykininPotent vasodilatorSynthase inhibitionSynthase inhibitorBradykininNitric oxideDependent mechanismReactive oxygen speciesHuman vasculatureSignificant increaseNitroprussideSubjectsOxygen species
2009
Endogenous Nitric Oxide Contributes to Bradykinin-Stimulated Glucose Uptake but Attenuates Vascular Tissue-Type Plasminogen Activator Release
Pretorius M, Brown NJ. Endogenous Nitric Oxide Contributes to Bradykinin-Stimulated Glucose Uptake but Attenuates Vascular Tissue-Type Plasminogen Activator Release. Journal Of Pharmacology And Experimental Therapeutics 2009, 332: 291-297. PMID: 19841473, PMCID: PMC2802470, DOI: 10.1124/jpet.109.160168.Peer-Reviewed Original ResearchConceptsT-PA releaseNet t-PA releaseForearm blood flowTissue-type plasminogen activator releaseL-NMMANitric oxide synthasePlasminogen activator releaseGlucose uptakeActivator releaseBaseline forearm blood flowBaseline forearm vascular resistanceArterial-venous gradientEndogenous NO contributesForearm vascular resistanceNitric oxide contributesIntra-arterial bradykininMonomethyl-L-arginineMuscle glucose uptakeCyclooxygenase inhibitor aspirinEndogenous nitric oxide contributesGender-stratified analysesVascular resistanceNondiabetic subjectsNOS inhibitionFibrinolytic response
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