2018
Angiotensin receptor blocker vs ACE inhibitor effects on HDL functionality in patients on maintenance hemodialysis
Kaseda R, Tsuchida Y, Gamboa JL, Zhong J, Zhang L, Yang H, Dikalova A, Bian A, Davies S, Fogo AF, Linton MF, Brown NJ, Ikizler TA, Kon V. Angiotensin receptor blocker vs ACE inhibitor effects on HDL functionality in patients on maintenance hemodialysis. Nutrition Metabolism And Cardiovascular Diseases 2018, 28: 582-591. PMID: 29691148, PMCID: PMC5959764, DOI: 10.1016/j.numecd.2018.02.020.Peer-Reviewed Original ResearchConceptsAngiotensin receptor blockersHigh-density lipoproteinToll-like receptorsAnti-inflammatory effectsReceptor blockersCytokine responsesActivation of TLRsSerum amyloid A (SAA) levelsACE inhibitor effectsHigh cardiovascular riskAdvanced kidney diseaseMaintenance hemodialysis patientsInflammatory cytokine responseAnti-oxidative effectsACEI treatmentAtheroprotective actionARB treatmentCardiovascular eventsMaintenance hemodialysisAngiotensin actionCardiovascular riskHemodialysis patientsCellular superoxide productionHDL functionalityKidney diseaseDipeptidyl 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
2013
The Effect of Reducing Maximum Shift Lengths to 16 Hours on Internal Medicine Interns’ Educational Opportunities
Theobald CN, Stover DG, Choma NN, Hathaway J, Green JK, Peterson NB, Sponsler KC, Vasilevskis EE, Kripalani S, Sergent J, Brown NJ, Denny JC. The Effect of Reducing Maximum Shift Lengths to 16 Hours on Internal Medicine Interns’ Educational Opportunities. Academic Medicine 2013, 88: 512-518. PMID: 23425987, PMCID: PMC3638874, DOI: 10.1097/acm.0b013e318285800f.Peer-Reviewed Original ResearchConceptsDuty hour restrictionsMaximum shift lengthsInternal medicine internsHour restrictionsVanderbilt University Medical CenterUniversity Medical CenterCommon presenting problemMedicine internsMore patientsUnique patientsInpatient encountersMorning report conferencesMedian numberMedical CenterProgress notesClinical exposureProcedural experienceShift lengthPresenting problemPatientsMore historyHoursExposureAttendanceInterns
2012
Aldosterone deficiency and mineralocorticoid receptor antagonism prevent angiotensin II–induced cardiac, renal, and vascular injury
Luther JM, Luo P, Wang Z, Cohen SE, Kim HS, Fogo AB, Brown NJ. Aldosterone deficiency and mineralocorticoid receptor antagonism prevent angiotensin II–induced cardiac, renal, and vascular injury. Kidney International 2012, 82: 643-651. PMID: 22622494, PMCID: PMC3434275, DOI: 10.1038/ki.2012.170.Peer-Reviewed Original ResearchMeSH KeywordsAldosteroneAngiotensin IIAnimalsAortaBiomarkersBlood PressureCytochrome P-450 CYP11B2Disease Models, AnimalFibrosisGene Expression RegulationHeart DiseasesInflammationKidney DiseasesKidney GlomerulusMiceMice, 129 StrainMice, Inbred C57BLMineralocorticoid Receptor AntagonistsMyocardiumReceptors, MineralocorticoidRenin-Angiotensin SystemSodium Chloride, DietarySpironolactoneTime FactorsVascular DiseasesConceptsMineralocorticoid receptor antagonismAbsence of aldosteroneAldosterone deficiencyAngiotensin IIReceptor antagonismMineralocorticoid receptorKnockout miceAldosterone synthase knockout (AS(-/-)) miceMineralocorticoid receptor antagonist spironolactonePlasminogen activator inhibitor-1 mRNA expressionAldosterone synthase inhibitionMineralocorticoid receptor activationPrevents angiotensin IIAngiotensin II treatmentSynthase knockout miceBlood urea nitrogenWild-type miceWild-type littermatesMineralocorticoid antagonismAntagonist spironolactoneAortic remodelingRenal injuryEndogenous aldosteroneGlomerular hypertrophyGlomerular injury
2011
Combined angiotensin-converting enzyme inhibition and receptor blockade associate with increased risk of cardiovascular death in hemodialysis patients
Chan KE, Ikizler TA, Gamboa JL, Yu C, Hakim RM, Brown NJ. Combined angiotensin-converting enzyme inhibition and receptor blockade associate with increased risk of cardiovascular death in hemodialysis patients. Kidney International 2011, 80: 978-985. PMID: 21775975, PMCID: PMC3656595, DOI: 10.1038/ki.2011.228.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAngiotensin II Type 1 Receptor BlockersAngiotensin-Converting Enzyme InhibitorsAntihypertensive AgentsCardiovascular DiseasesDrug Therapy, CombinationFemaleHumansHypertensionKaplan-Meier EstimateKidney Failure, ChronicLogistic ModelsMaleMiddle AgedPropensity ScoreProportional Hazards ModelsRenal DialysisRetrospective StudiesRisk AssessmentRisk FactorsSurvival RateTime FactorsTreatment OutcomeUnited StatesConceptsAngiotensin receptor blockersAntihypertensive medicationsARB therapyCardiovascular deathChronic hemodialysisCardiovascular mortalityHazard ratioHemodialysis patientsRisk factorsBaseline cardiovascular risk factorsAngiotensin-converting enzyme inhibitionLarge dialysis providerCardiovascular risk factorsChronic hemodialysis patientsKaplan-Meier methodMortality hazard ratioAntihypertensive therapyReceptor blockersAntihypertensive agentsCox regressionCerebrovascular mortalityClinical trialsTreatment weightingObservational studyACEIThis is not Dr. Conn's aldosterone anymore.
Brown NJ. This is not Dr. Conn's aldosterone anymore. Transactions Of The American Clinical And Climatological Association 2011, 122: 229-43. PMID: 21686229, PMCID: PMC3116341.Peer-Reviewed Original ResearchMeSH KeywordsAldosteroneAngiotensin IIAngiotensin II Type 1 Receptor BlockersAngiotensin-Converting Enzyme InhibitorsAnimalsBlood PressureCytochrome P-450 CYP11B2Disease Models, AnimalEnzyme InhibitorsFibrosisGene Expression RegulationHumansHyperaldosteronismInflammation MediatorsKidneyLigandsMiceMineralocorticoid Receptor AntagonistsMyocardiumRatsReceptors, MineralocorticoidSignal TransductionTime FactorsConceptsMR-independent pathwayPrevalence of hyperaldosteronismAngiotensin receptor blockersMineralocorticoid receptor antagonismSecretion of aldosteroneAldosterone-secreting adenomasPro-fibrotic effectsReceptor blockersResistant hypertensionSevere hypertensionAldosterone concentrationRenal injuryEndogenous aldosteroneACE inhibitorsCardiovascular remodelingAngiotensin IIReceptor antagonismHeart diseaseProfibrotic effectsAldosteroneBaseline valuesEnzyme inhibitorsPatientsPotassium homeostasisHypertension
2008
Endogenous Aldosterone Contributes to Acute Angiotensin II-Stimulated Plasminogen Activator Inhibitor-1 and Preproendothelin-1 Expression in Heart But Not Aorta
Luther JM, Wang Z, Ma J, Makhanova N, Kim HS, Brown NJ. Endogenous Aldosterone Contributes to Acute Angiotensin II-Stimulated Plasminogen Activator Inhibitor-1 and Preproendothelin-1 Expression in Heart But Not Aorta. Endocrinology 2008, 150: 2229-2236. PMID: 19106220, PMCID: PMC2671907, DOI: 10.1210/en.2008-1296.Peer-Reviewed Original ResearchConceptsPpET-1 expressionAng IIPlasminogen activator inhibitor-1Profibrotic gene expressionEndogenous aldosteroneActivator inhibitor-1PAI-1MRNA expressionWT miceAngiotensin IITGF-beta mRNA expressionInhibitor-1Acute angiotensin IIBasal PAI-1Plasma renin activityAcute stimulatory effectPpET-1 mRNA expressionTGF-beta expressionTissue mRNA expressionPreproendothelin-1 expressionRenin activityAldosterone concentrationH infusionAldosteronePpET-1
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 concentration
2000
Inhibition of aminopeptidase P potentiates wheal response to bradykinin in angiotensin-converting enzyme inhibitor-treated humans.
Kim KS, Kumar S, Simmons WH, Brown NJ. Inhibition of aminopeptidase P potentiates wheal response to bradykinin in angiotensin-converting enzyme inhibitor-treated humans. Journal Of Pharmacology And Experimental Therapeutics 2000, 292: 295-8. PMID: 10604961.Peer-Reviewed Original ResearchConceptsDegradation of bradykininACE inhibitionWheal responseACE inhibitor quinaprilEffect of quinaprilNon-ACE pathwaysMetabolism of bradykininDose-response curveCardioprotective effectsIntradermal administrationIntradermal injectionOral administrationHealthy subjectsEnzyme inhibitorsSignificant interactionQuinaprilBradykininAminopeptidase PAngiotensinInhibitionAdministrationHuman skinPresent studyApstatinResponse
1999
Clinical Experience Over 48 Years With Pheochromocytoma
Goldstein R, O’Neill J, Holcomb G, Morgan W, Neblett W, Oates J, Brown N, Nadeau J, Smith B, Page D, Abumrad N, Scott H. Clinical Experience Over 48 Years With Pheochromocytoma. Annals Of Surgery 1999, 229: 755. PMID: 10363888, PMCID: PMC1420821, DOI: 10.1097/00000658-199906000-00001.Peer-Reviewed Original ResearchConceptsMicroscopic malignant featuresExtraadrenal pheochromocytomaMalignant diseaseMalignant featuresAdrenal pheochromocytomaSurgical managementMultiple endocrine neoplasia type 2Von Hippel-Lindau diseasePatient's malignant diseaseSame overall survivalLong-term outcomesRate of malignancyKaplan-Meier survival distributionsNumber of patientsVon Recklinghausen's diseaseHippel-Lindau diseaseAreas of controversyCarney syndromeAdrenal tumorsOverall survivalMale patientsFemale patientsBenign diseasePatient survivalFormer tumor
1991
A pharmacodynamic interaction between caffeine and phenylpropanolamine
Brown N, Ryder D, Branch R. A pharmacodynamic interaction between caffeine and phenylpropanolamine. Clinical Pharmacology & Therapeutics 1991, 50: 363-371. PMID: 1914371, DOI: 10.1038/clpt.1991.152.Peer-Reviewed Original ResearchConceptsBlood pressurePharmacodynamic interactionsPlasma renin activityRenin-angiotensin systemDrug-free subjectsCoadministration of caffeineRenin responseRenin activityPharmacokinetic interactionsCatecholamine levelsSupine positionNormal subjectsLatin square design studyDrug AdministrationRandom orderPhenylpropanolamineMetabolite levelsPlaceboCaffeineSubjectsAdditive increaseHoursCoadministrationEpinephrineAdministrationCaffeine potentiates the renin response to diazoxide in man. Evidence for a regulatory role of endogenous adenosine.
Brown NJ, Porter J, Ryder D, Branch RA. Caffeine potentiates the renin response to diazoxide in man. Evidence for a regulatory role of endogenous adenosine. Journal Of Pharmacology And Experimental Therapeutics 1991, 256: 56-61. PMID: 1988669.Peer-Reviewed Original ResearchConceptsRenin responseEndogenous adenosineRenin releaseDiazoxide infusionAdenosine inhibitsRegulation of reninCross-over studyAdministration of diazoxideAdenosine receptor blockerModest tachycardiaPRA responseReceptor blockersBP responseLoading dosePRA measurementsContinuous infusionNormal subjectsStudy daysDiazoxideMaximal pulseInfusionPresence of caffeineReninCaffeineAdenosine