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
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
2001
Plasminogen Activator Inhibitor-1 Deficiency Prevents Hypertension and Vascular Fibrosis in Response to Long-term Nitric Oxide Synthase Inhibition
Kaikita K, Fogo A, Ma L, Schoenhard J, Brown N, Vaughan D. Plasminogen Activator Inhibitor-1 Deficiency Prevents Hypertension and Vascular Fibrosis in Response to Long-term Nitric Oxide Synthase Inhibition. Circulation 2001, 104: 839-844. PMID: 11502712, DOI: 10.1161/hc3301.092803.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlood PressureBody WeightCollagenCoronary VesselsEnzyme InhibitorsFibrosisHemodynamicsHypertensionHypertrophy, Left VentricularMaleMiceMice, Inbred C57BLMice, KnockoutNG-Nitroarginine Methyl EsterNitric Oxide SynthasePlasminogen Activator Inhibitor 1Reverse Transcriptase Polymerase Chain ReactionRNA, MessengerTimeConceptsPlasminogen activator inhibitor-1Systolic blood pressureLong-term NOS inhibitionBlood pressurePAI-1 deficiencyNitric oxide synthaseCoronary perivascular fibrosisPerivascular fibrosisNOS inhibitionWT miceLong-term nitric oxide synthase inhibitionNitro-L-arginine methyl esterNitric oxide synthase inhibitionWild-type male miceControl WT miceStructural vascular changesOxide synthase inhibitionArteriosclerotic cardiovascular diseaseDevelopment of fibrosisPAI-1 activityNew therapeutic strategiesActivator inhibitor-1Cardiac type ILong-term inhibitionPrevents hypertension