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
2007
Dipeptidyl peptidase IV deficiency increases susceptibility to angiotensin-converting enzyme inhibitor–induced peritracheal edema
Byrd JB, Shreevatsa A, Putlur P, Foretia D, McAlexander L, Sinha T, Does MD, Brown NJ. Dipeptidyl peptidase IV deficiency increases susceptibility to angiotensin-converting enzyme inhibitor–induced peritracheal edema. Journal Of Allergy And Clinical Immunology 2007, 120: 403-408. PMID: 17531305, DOI: 10.1016/j.jaci.2007.04.012.Peer-Reviewed Original ResearchConceptsACE inhibitor-associated angioedemaDPPIV-deficient ratsMagnetic resonance imagingEdema formationSubstance PSerum dipeptidyl peptidase IV activityResonance imagingCaptopril-treated ratsSaline-treated ratsReceptor-dependent mechanismDipeptidyl peptidase IV activityPeptidase IV activityACE inhibitionSerial T2F344 ratsAnimal modelsEdemaAngioedemaDPPIV activityRatsDipeptidyl peptidase activityImpaired degradationSpantideDeficiencyMagnetic resonance
2006
Angiotensin II Induces Interleukin-6 in Humans Through a Mineralocorticoid Receptor–Dependent Mechanism
Luther JM, Gainer JV, Murphey LJ, Yu C, Vaughan DE, Morrow JD, Brown NJ. Angiotensin II Induces Interleukin-6 in Humans Through a Mineralocorticoid Receptor–Dependent Mechanism. Hypertension 2006, 48: 1050-1057. PMID: 17043157, DOI: 10.1161/01.hyp.0000248135.97380.76.Peer-Reviewed Original ResearchConceptsMineralocorticoid receptor-dependent mechanismAngiotensin IIReceptor-dependent mechanismBlood pressureIL-6Normotensive subjectsCrossover studyHigh-sensitivity C-reactive proteinSerum IL-6 concentrationDouble-blind crossover studyOxidative stressWeeks of placeboIL-6 concentrationsC-reactive proteinRenal plasma flowIntravenous aldosteroneAldosterone responseSerum potassiumInterleukin-6Mineralocorticoid receptorPlaceboAldosteroneSpironolactoneSeparate daysReceptor independent
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
2002
Smoking Impairs Bradykinin-Stimulated t-PA Release
Pretorius M, Rosenbaum DA, Lefebvre J, Vaughan DE, Brown NJ. Smoking Impairs Bradykinin-Stimulated t-PA Release. Hypertension 2002, 39: 767-771. PMID: 11897760, DOI: 10.1161/hy0302.105767.Peer-Reviewed Original ResearchConceptsTissue plasminogen activator releaseTissue plasminogen activator responsePlasminogen activator releaseForearm blood flowDose-dependent increaseActivator releaseBlood flowDoses of nitroprussideSignificant dose-dependent increaseActivator responseStrain-gauge plethysmographyBody mass indexEffect of bradykininT-PA releaseReceptor-dependent mechanismEndothelial functionBrachial arteryMass indexMethacholineSmokersNonsmokersBradykininHuman endotheliumRandom orderSignificant differences