2022
DPP4 (Dipeptidyl Peptidase-4) Inhibition Increases Catecholamines Without Increasing Blood Pressure During Sustained ACE (Angiotensin-Converting Enzyme) Inhibitor Treatment
Wilson JR, Garner EM, Mashayekhi M, Hubers SA, Bustamante C, Kerman SJ, Nian H, Shibao CA, Brown NJ. DPP4 (Dipeptidyl Peptidase-4) Inhibition Increases Catecholamines Without Increasing Blood Pressure During Sustained ACE (Angiotensin-Converting Enzyme) Inhibitor Treatment. Hypertension 2022, 79: 827-835. PMID: 35045722, PMCID: PMC8917054, DOI: 10.1161/hypertensionaha.121.18348.Peer-Reviewed Original ResearchMeSH KeywordsAdultAngiotensin Receptor AntagonistsAngiotensin-Converting Enzyme InhibitorsAngiotensinsAprepitantBlood PressureCardiovascular AgentsCatecholaminesCross-Over StudiesDiabetes Mellitus, Type 2Dipeptidyl Peptidase 4HumansNorepinephrineRamiprilRenin-Angiotensin SystemSitagliptin PhosphateValsartanConceptsDPP4 inhibitionBlood pressureACE inhibitionDouble-blind crossover studyAcute ACE inhibitionBlood pressure armNK1 receptor blockerACE inhibitor treatmentOral diabetes medicationsCalcium channel blockersType 2 diabetesEffects of DPP4Aldosterone systemCardiovascular complicationsDiabetes medicationsReceptor blockersCardiovascular effectsCrossover therapyHeart failureHypotensive effectCrossover studyChannel blockersDPP4 inhibitorsHeart rateInhibitor treatment
2021
Active B-Type Natriuretic Peptide Measured by Mass Spectrometry and Response to Sacubitril/Valsartan
Dillon EM, Wei SD, Gupta DK, Nian H, Rodibaugh BS, Bachmann KN, Naftilan AJ, Stevenson LW, Brown NJ. Active B-Type Natriuretic Peptide Measured by Mass Spectrometry and Response to Sacubitril/Valsartan. Journal Of Cardiac Failure 2021, 27: 1231-1239. PMID: 34133968, PMCID: PMC8578199, DOI: 10.1016/j.cardfail.2021.05.026.Peer-Reviewed Original ResearchConceptsSacubitril/valsartanSacubitril/valsartan treatmentHeart failureBNP1-32NT-proBNPValsartan treatmentActive B-type natriuretic peptideEnd-stage renal diseaseB-type natriuretic peptideNT-proBNP immunoassaysPg/mLRenal diseaseNatriuretic peptideBNP productionHealthy volunteersBNPPg/ValsartanPatientsInhibition of degradationPeptide immunoassayBNP degradationTreatmentImmunoassayMS accounts
2019
Dipeptidyl Peptidase 4 Inhibition Increases Postprandial Norepinephrine via Substance P (NK1 Receptor) During RAAS Inhibition
Wilson JR, Kerman SJ, Hubers SA, Yu C, Nian H, Grouzmann E, Eugster PJ, Mayfield DS, Brown NJ. Dipeptidyl Peptidase 4 Inhibition Increases Postprandial Norepinephrine via Substance P (NK1 Receptor) During RAAS Inhibition. Journal Of The Endocrine Society 2019, 3: 1784-1798. PMID: 31528826, PMCID: PMC6734191, DOI: 10.1210/js.2019-00185.Peer-Reviewed Original ResearchPostprandial blood pressureDPP4 inhibitionNPY 1Blood pressureHeart failureACE inhibitionSubstance PVasoactive peptidesPostprandial glucagon-like peptide-1Substance P receptor blockadeDipeptidyl peptidase-4 inhibitorsGlucagon-like peptide-1Mixed-meal studyAngiotensin receptor blockersDouble-blind treatmentPeptidase-4 inhibitorsType 2 diabetesReceptor-dependent mechanismAntihypertensive groupNPY 3Y1 agonistRAAS inhibitionReceptor blockersReceptor blockadeACE inhibitors
2018
Early urine electrolyte patterns in patients with acute heart failure
Collins SP, Jenkins CA, Baughman A, Miller KF, Storrow AB, Han JH, Brown NJ, Liu D, Luther JM, McNaughton CD, Self WH, Peng D, Testani JM, Lindenfeld J. Early urine electrolyte patterns in patients with acute heart failure. ESC Heart Failure 2018, 6: 80-88. PMID: 30295437, PMCID: PMC6351901, DOI: 10.1002/ehf2.12368.Peer-Reviewed Original ResearchConceptsAcute heart failureDiuretic administrationDiuretic resistanceHeart failureLoop diureticsLow urinary sodiumEscalation of therapyUrine sodium excretionSubset of patientsSystolic blood pressureEmergency department patientsUrine sodium concentrationAHF diagnosisAHF patientsIntravenous diureticsUrinary sodiumED staySodium excretionUrinary electrolytesUrine sodiumNatriuretic responseStandard therapyBlood pressureDepartment patientsUrine outputDPP (Dipeptidyl Peptidase)-4 Inhibition Potentiates the Vasoconstrictor Response to NPY (Neuropeptide Y) in Humans During Renin-Angiotensin-Aldosterone System Inhibition
Hubers SA, Wilson JR, Yu C, Nian H, Grouzmann E, Eugster P, Shibao CA, Billings FT, Jafarian Kerman S, Brown NJ. DPP (Dipeptidyl Peptidase)-4 Inhibition Potentiates the Vasoconstrictor Response to NPY (Neuropeptide Y) in Humans During Renin-Angiotensin-Aldosterone System Inhibition. Hypertension 2018, 72: 712-719. PMID: 29987109, PMCID: PMC6202157, DOI: 10.1161/hypertensionaha.118.11498.Peer-Reviewed Original ResearchConceptsNPY infusionPlacebo-controlled crossover studyAngiotensin-converting enzyme inhibitorAldosterone system inhibitionDose-dependent vasoconstrictionIntra-arterial enalaprilatAngiotensin receptor blockersForearm blood flowHigh-risk patientsOrder of treatmentReceptor blockersVasoconstrictor effectVasoconstrictor responsesCardiovascular effectsRenin-AngiotensinBrachial arteryHeart failureNorepinephrine releaseCrossover studyEndogenous NPYY1 receptorCrossover treatmentSystem inhibitionY2 receptorsDPP4 inhibition
2016
Risk for Hospitalized Heart Failure Among New Users of Saxagliptin, Sitagliptin, and Other Antihyperglycemic Drugs: A Retrospective Cohort Study.
Toh S, Hampp C, Reichman ME, Graham DJ, Balakrishnan S, Pucino F, Hamilton J, Lendle S, Iyer A, Rucker M, Pimentel M, Nathwani N, Griffin MR, Brown NJ, Fireman BH. Risk for Hospitalized Heart Failure Among New Users of Saxagliptin, Sitagliptin, and Other Antihyperglycemic Drugs: A Retrospective Cohort Study. Annals Of Internal Medicine 2016, 164: 705-14. PMID: 27110660, PMCID: PMC5178978, DOI: 10.7326/m15-2568.Peer-Reviewed Original ResearchConceptsHospitalized heart failureMini-Sentinel programCohort studyHeart failureAntihyperglycemic agentsPropensity score-matched analysisDipeptidyl peptidase-4 inhibitorsNew-user cohort studyU.S. FoodPrior cardiovascular diseaseRetrospective cohort studyPeptidase-4 inhibitorsSubgroup of patientsPrincipal discharge diagnosisDPP-4 inhibitorsSecond-generation sulfonylureasType 2 diabetesLarge cohort studyDisease risk scoreSitagliptin usersStudy drugHazard ratioDischarge diagnosisNinth RevisionResidual confoundingCombined 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
2014
Hypertension Is Associated With Preamyloid Oligomers in Human Atrium: A Missing Link in Atrial Pathophysiology?
Sidorova TN, Mace LC, Wells KS, Yermalitskaya LV, Su P, Shyr Y, Atkinson JB, Fogo AB, Prinsen JK, Byrne JG, Petracek MR, Greelish JP, Hoff SJ, Ball SK, Glabe CG, Brown NJ, Barnett JV, Murray KT. Hypertension Is Associated With Preamyloid Oligomers in Human Atrium: A Missing Link in Atrial Pathophysiology? Journal Of The American Heart Association 2014, 3: e001384. PMID: 25468655, PMCID: PMC4338732, DOI: 10.1161/jaha.114.001384.Peer-Reviewed Original ResearchConceptsAtrial samplesAtrial amyloidosisMitral valve replacement/repairValve replacement/repairCoronary Artery Bypass GraftingHuman atriumArtery Bypass GraftingElective cardiac surgeryAortic valve replacementPresence of hypertensionCongestive heart failureCoronary artery diseaseAtrial natriuretic peptideReplacement/repairAtrial pathophysiologyBypass GraftingClinical hypertensionMost patientsValve replacementArtery diseaseCardiac surgeryHeart failureNatriuretic peptideAtrial arrhythmiasMean age
2005
Aldosterone and end-organ damage
Brown N. Aldosterone and end-organ damage. Current Opinion In Internal Medicine 2005, 4: 381-387. DOI: 10.1097/00132980-200508000-00009.Peer-Reviewed Original ResearchMineralocorticoid receptor antagonismCongestive heart failureHeart failureReceptor antagonismMineralocorticoid receptorOxidative stressMineralocorticoid receptor-dependent mechanismEndothelial nitric oxide synthaseContribution of aldosteroneEnd-organ damageReceptor-independent effectsMineralocorticoid receptor agonistRecent clinical studiesInduction of inflammationNitric oxide synthaseRapid nongenomic mechanismsReceptor-dependent mechanismPurpose of reviewExtracellular matrix turnoverMineralocorticoid antagonismInflammatory markersCardiovascular mortalityEndothelial dysfunctionRenal injuryEndothelial functionAldosterone and end-organ damage
Brown NJ. Aldosterone and end-organ damage. Current Opinion In Nephrology & Hypertension 2005, 14: 235-241. PMID: 15821416, DOI: 10.1097/01.mnh.0000165889.60254.98.Peer-Reviewed Original ResearchConceptsMineralocorticoid receptor antagonismCongestive heart failureHeart failureReceptor antagonismMineralocorticoid receptorOxidative stressMineralocorticoid receptor-dependent mechanismEndothelial nitric oxide synthaseContribution of aldosteroneEnd-organ damageReceptor-independent effectsMineralocorticoid receptor agonistRecent clinical studiesInduction of inflammationNitric oxide synthaseRapid nongenomic mechanismsReceptor-dependent mechanismExtracellular matrix turnoverMineralocorticoid antagonismInflammatory markersCardiovascular mortalityEndothelial dysfunctionRenal injuryEndothelial functionRenal disease
2003
Eplerenone
Brown NJ. Eplerenone. Circulation 2003, 107: 2512-2518. PMID: 12756192, DOI: 10.1161/01.cir.0000071081.35693.9a.Peer-Reviewed Original ResearchConceptsAldosterone receptor antagonistsReceptor antagonistMineralocorticoid receptor-dependent mechanismSelective aldosterone receptor antagonistAldosterone receptor antagonismRole of aldosteroneCongestive heart failureTreatment of hypertensionReceptor-dependent mechanismAntiandrogenic side effectsRenal injuryHeart failureReceptor antagonismCardiovascular toxicityClinical trialsSide effectsAnimal studiesEplerenoneAldosteroneAntagonistHypertensionPatientsSpironolactoneInjuryMortality
1998
Angiotensin-Converting Enzyme Inhibitors
Brown N, Vaughan D. Angiotensin-Converting Enzyme Inhibitors. Circulation 1998, 97: 1411-1420. PMID: 9577953, DOI: 10.1161/01.cir.97.14.1411.Peer-Reviewed Original ResearchConceptsACE inhibitorsVentricular dysfunctionMyocardial infarctionAngiotensin AT1 receptor antagonistAngiotensin converting enzyme (ACE) inhibitorsTissue-bound ACESystemic vascular resistanceCongestive heart failureAT1 receptor antagonistTreatment of hypertensionRoute of eliminationVascular resistanceCardiovascular mortalityDiabetic nephropathyEssential hypertensionHeart failureNatriuretic propertiesRenal diseaseVasoactive substancesAngiotensin IIReceptor antagonistHeart rateSide effectsEnzyme inhibitorsHypertrophic properties