2000
Temporal Events Underlying Arterial Remodeling After Chronic Flow Reduction in Mice
Rudic R, Bucci M, Fulton D, Segal S, Sessa W. Temporal Events Underlying Arterial Remodeling After Chronic Flow Reduction in Mice. Circulation Research 2000, 86: 1160-1166. PMID: 10850968, DOI: 10.1161/01.res.86.11.1160.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarotid Artery, CommonCell DeathDrug CombinationsIn Vitro TechniquesMaleMiceMice, Inbred C57BLMuscle, Smooth, VascularNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIRegional Blood FlowTime FactorsTunica MediaVasodilator AgentsVasomotor SystemConceptsLeft common carotid arteryRight common carotid arteryCommon carotid arteryCarotid arteryBlood flowLeft external carotid arteryEndothelial NO synthase (eNOS) functionEndothelial NO synthase (eNOS) mRNAExternal carotid arteryNO synthase mRNANitrovasodilator sodium nitroprussideAcute ligationEndothelial dysfunctionArterial remodelingControl arteriesVascular remodelingAdult miceSodium nitroprussideDay 7Structural remodelingArteryLuminal remodelingMarked reductionProtein levelsMice
1999
Hsp90 regulation of endothelial nitric oxide synthase contributes to vascular control in portal hypertension
Shah V, Wiest R, Garcia-Cardena G, Cadelina G, Groszmann R, Sessa W. Hsp90 regulation of endothelial nitric oxide synthase contributes to vascular control in portal hypertension. American Journal Of Physiology 1999, 277: g463-g468. PMID: 10444461, DOI: 10.1152/ajpgi.1999.277.2.g463.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcholineAnimalsBenzoquinonesBlood VesselsHSP90 Heat-Shock ProteinsHypertension, PortalIn Vitro TechniquesLactams, MacrocyclicMaleMethoxamineMicrocirculationNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IIIQuinonesRatsRats, Sprague-DawleySplanchnic CirculationTissue DistributionVasoconstrictor AgentsVasodilationVasodilator AgentsConceptsEndothelial nitric oxide synthasePortal vein ligationNitric oxide synthasePortal hypertensionMesenteric vasculatureOxide synthaseNormal animalsACh-dependent vasodilationExperimental portal hypertensionExcessive NO productionNO-dependent responsesNOS catalytic activityDependent vasodilationVein ligationVascular controlMesenteric circulationPVL animalsMesenteric vesselsHeat shock protein 90Sodium nitroprussideNO productionEndothelial liningHypertensionShock protein 90Methoxamine
1991
Inhibition of human platelet aggregation by endothelium-derived relaxing factor, sodium nitroprusside or iloprost is potentiated by captopril and reduced thiols.
Mollace V, Salvemini D, Sessa W, Vane J. Inhibition of human platelet aggregation by endothelium-derived relaxing factor, sodium nitroprusside or iloprost is potentiated by captopril and reduced thiols. Journal Of Pharmacology And Experimental Therapeutics 1991, 258: 820-3. PMID: 1716310.Peer-Reviewed Original ResearchConceptsPlatelet aggregationSodium nitroprussideAntiaggregatory effectAngiotensin-converting enzyme inhibitorOxygen-derived free radicalsInhibitors of angiotensinHuman platelet aggregationSulfhydryl-containing compoundsCyclic AMP levelsPlatelet cyclic GMPAggregatory responsePotentiating effectTeprotideAntiplatelet compoundsEnzyme inhibitorsEnalaprilatAntiaggregatory propertiesAMP levelsIloprostEndothelial cellsIntracellular scavengerNitroprussideCyclic GMPNACBovine aorta