2015
Dietary salt regulates epithelial sodium channels in rat endothelial cells: adaptation of vasculature to salt
Liu H, Zhang J, Sun Y, Li X, Jiang S, Liu M, Shi J, Song B, Zhao D, Ma H, Zhang Z. Dietary salt regulates epithelial sodium channels in rat endothelial cells: adaptation of vasculature to salt. British Journal Of Pharmacology 2015, 172: 5634-5646. PMID: 25953733, PMCID: PMC4667865, DOI: 10.1111/bph.13185.Peer-Reviewed Original ResearchConceptsEndothelium-dependent relaxationWeeks of HS dietEpithelial sodium channelMesenteric arteryENaC activityEndothelial ENaCEndothelial cellsHS dietSprague-DawleyEnhancement of endothelium-dependent relaxationSodium channelsSecond-order mesenteric arteriesBlocker of ENaCWire myograph assayPatch-clamp techniquePlasma aldosterone levelsSalt-sensitive hypertensionResponse to AChNegative modulatorRat endothelial cellsModulation of vasodilationVascular endothelial cellsFunctional ENaCENaC expressionRelease of NO
2007
Vascular endothelial dysfunction in cirrhosis
Iwakiri Y, Groszmann RJ. Vascular endothelial dysfunction in cirrhosis. Journal Of Hepatology 2007, 46: 927-934. PMID: 17391799, DOI: 10.1016/j.jhep.2007.02.006.BooksConceptsEndothelium-dependent relaxationEndothelial dysfunctionSinusoidal endothelial cellsPortal hypertensionVascular nitric oxide levelsVascular endothelial dysfunctionNitric oxide levelsSEC dysfunctionVascular resistanceEarly key eventSplanchnic circulationLiver cirrhosisVasodilator moleculeLiver microcirculationSystemic circulationOxide levelsCirrhosisDysfunctionEndothelial cellsHypertensionMultiple diseasesKey eventsArteryMicrocirculationDisease
2000
Modulation of Nitric-Oxide Synthase by Nicotine 1 1 This study was funded by grants from the American Heart Association (AHA 96-010290), the Mayo Graduate School of Medicine, and the Mayo Foundation.
Tonnessen B, Severson S, Hurt R, Miller V. Modulation of Nitric-Oxide Synthase by Nicotine 1 1 This study was funded by grants from the American Heart Association (AHA 96-010290), the Mayo Graduate School of Medicine, and the Mayo Foundation. Journal Of Pharmacology And Experimental Therapeutics 2000, 295: 601-606. PMID: 11046094, DOI: 10.1016/s0022-3565(24)38944-x.Peer-Reviewed Original ResearchConceptsEndothelial nitric oxide synthaseRecombinant endothelial nitric oxide synthaseEffects of nicotineNitric oxide synthaseAortic endothelial cellsNitric oxideInducible NOSNeuronal NOSEndothelium-derived nitric oxideEndothelial cellsEndothelium-dependent relaxationCalcium-dependent accumulationPresence of nicotineUntreated dogsNicotine administrationM nicotineNOS activityNicotine doseNOSNicotineCitrulline accumulationInconsistent findingsConcentration of NADPHCitrullineAccumulation of citrullineTime and dose effect of transdermal nicotine on endothelial function
Miller V, Clouse W, Tonnessen B, Boston U, Severson S, Bonde S, Rud K, Hurt R. Time and dose effect of transdermal nicotine on endothelial function. AJP Heart And Circulatory Physiology 2000, 279: h1913-h1921. PMID: 11009480, DOI: 10.1152/ajpheart.2000.279.4.h1913.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine DiphosphateAdministration, CutaneousAnimalsAortaCalcimycinCalciumCoronary VesselsCotinineDogsDose-Response Relationship, DrugEndothelium, VascularEnzyme InhibitorsIn Vitro TechniquesIonophoresMaleNicotineNitratesNitric Oxide SynthaseNitritesomega-N-MethylarginineRNA, MessengerTime FactorsVasodilationConceptsEndothelium-dependent responsesEndothelium-dependent relaxationNicotine patchNicotine treatmentNitric oxideNicotine patch therapyEffects of nicotineBiphasic dose effectDose effectCalcium ionophore AAortic endothelial cellsTransdermal nicotineEndothelial functionPatch therapyCoronary arteryCounter medicationsCessation programsNOS activityAdrenergic agonistsNOS mRNAIonophore AIsometric forceEndothelial cellsNicotineDose rangeGeldanamycin, an inhibitor of heat shock protein 90 (Hsp90) mediated signal transduction has anti‐inflammatory effects and interacts with glucocorticoid receptor in vivo
Bucci M, Roviezzo F, Cicala C, Sessa W, Cirino G. Geldanamycin, an inhibitor of heat shock protein 90 (Hsp90) mediated signal transduction has anti‐inflammatory effects and interacts with glucocorticoid receptor in vivo. British Journal Of Pharmacology 2000, 131: 13-16. PMID: 10960063, PMCID: PMC1572305, DOI: 10.1038/sj.bjp.0703549.Peer-Reviewed Original ResearchConceptsAnti-inflammatory effectsAnti-inflammatory actionEdema formationRU 486Heat shock protein 90Shock protein 90Endothelial nitric oxide synthaseEndothelium-dependent relaxationAnti-inflammatory dosePotential anti-inflammatory drugsVascular endothelial growth factorNitric oxide synthaseAnti-inflammatory drugsEndothelial growth factorDose-dependent mannerProtein 90Specific inhibitorIntact blood vesselsIntraplantar administrationPaw edemaMiddle arteryOxide synthaseRat aortaTherapeutic rationaleGlucocorticoid receptor
1999
Serotonin-Induced Coronary Contraction Increases After Blood Cardioplegia-Reperfusion
Métais C, Li J, Li J, Simons M, Sellke F. Serotonin-Induced Coronary Contraction Increases After Blood Cardioplegia-Reperfusion. Circulation 1999, 100: ii-328-ii-334. PMID: 10567324, DOI: 10.1161/01.cir.100.suppl_2.ii-328.Peer-Reviewed Original ResearchConceptsAtrial arteriolesBlood cardioplegiaVasomotor regulationSubstance PCOX-2Constitutive endothelial nitric oxide synthaseNitric oxideEndothelial nitric oxide synthaseCoronary microvascular regulationHyperkalemic blood cardioplegiaPotent contractile responseEndothelium-independent relaxationCoronary artery surgeryCoronary bypass surgeryEndothelium-dependent relaxationCoronary artery diseaseNitric oxide synthaseReverse transcriptase-polymerase chain reactionRelease of prostaglandinsBrief reperfusionCoronary contractionArtery surgeryCoronary spasmBypass surgeryContractile responseSerotonin-Induced Coronary Contraction Increases After Blood Cardioplegia-Reperfusion
Métais C, Li J, Li J, Simons M, Sellke F. Serotonin-Induced Coronary Contraction Increases After Blood Cardioplegia-Reperfusion. Circulation 1999, 100 DOI: 10.1161/circ.100.suppl_2.ii-328.Peer-Reviewed Original ResearchAtrial arteriolesBlood cardioplegiaVasomotor regulationSubstance PCOX-2Constitutive endothelial nitric oxide synthaseNitric oxideEndothelial nitric oxide synthaseCoronary microvascular regulationHyperkalemic blood cardioplegiaPotent contractile responseEndothelium-independent relaxationCoronary artery surgeryCoronary bypass surgeryEndothelium-dependent relaxationCoronary artery diseaseNitric oxide synthaseReverse transcriptase-polymerase chain reactionRelease of prostaglandinsBrief reperfusionArtery surgeryCoronary spasmBypass surgeryContractile responseVascular reactivityEffect of sialyl Lewisx oligosaccharide on myocardial and cerebral injury in the pig
Tofukuji M, Metais C, Collard C, Morse D, Stahl G, Nelson D, Li J, Simons M, Sellke F. Effect of sialyl Lewisx oligosaccharide on myocardial and cerebral injury in the pig. The Annals Of Thoracic Surgery 1999, 67: 112-119. PMID: 10086534, DOI: 10.1016/s0003-4975(98)01130-8.Peer-Reviewed Original ResearchConceptsArtery blood flowCardiopulmonary bypassMyeloperoxidase activityBrain arteriolesNeutrophil infiltrationOrgan perfusionBlood flowInducible isoformInternal carotid artery blood flowEndothelium-dependent relaxation responsesCoronary artery blood flowCarotid artery blood flowLeft ventricular systolic pressureNitric oxide synthase mRNAAdministration of CYBeneficial acute effectsCerebral vascular resistanceEndothelium-independent relaxationEndothelium-dependent relaxationVentricular systolic pressureCoronary artery occlusionMyocardial contractile functionNormothermic cardiopulmonary bypassLeft ventricular pressureNitric oxide synthase
1998
Anti-C5a monoclonal antibody reduces cardiopulmonary bypass and cardioplegia-induced coronary endothelial dysfunction
Tofukuji M, Stahl G, Agah A, Metais C, Simons M, Sellke F, This study was supported by National Institutes of Health grants HL46716 H. Anti-C5a monoclonal antibody reduces cardiopulmonary bypass and cardioplegia-induced coronary endothelial dysfunction. Journal Of Thoracic And Cardiovascular Surgery 1998, 116: 1060-1068. PMID: 9832699, DOI: 10.1016/s0022-5223(98)70059-5.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalCardiopulmonary BypassChemotaxis, LeukocyteComplement C5aCoronary VesselsEndothelium, VascularFemaleHeart Arrest, InducedHemodynamicsMaleMiceMice, Inbred BALB CMyocardial Reperfusion InjuryNeutrophilsNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIPeroxidaseSwineConceptsEndothelium-dependent relaxationSaline solution groupCardiopulmonary bypassMonoclonal antibodiesCardioplegic reperfusionSolution groupImpaired endothelium-dependent relaxationAnti-C5a monoclonal antibodyCoronary endothelial dysfunctionPolymorphonuclear leukocyte infiltrationLeft ventricular pressureSaline solution vehiclePercent segmental shorteningMonoclonal antibody groupC5a inhibitionEndothelial dysfunctionMyeloperoxidase activityCoronary arteriolesLeukocyte infiltrationSegmental shorteningCoronary arteryHyperkalemic cardioplegiaFunctional preservationVentricular pressureVascular studies
1996
Angiogenesis induced by acidic fibroblast growth factor as an alternative method of revascularization for chronic myocardial ischemia
Sellke F, Li J, Stamler A, Lopez J, Thomas K, Simons M. Angiogenesis induced by acidic fibroblast growth factor as an alternative method of revascularization for chronic myocardial ischemia. Surgery 1996, 120: 182-188. PMID: 8751581, DOI: 10.1016/s0039-6060(96)80286-8.Peer-Reviewed Original ResearchConceptsCollateral-dependent LCx regionAcidic fibroblast growth factorFibroblast growth factorLCx regionBlood flowSodium nitroprussideProximal left circumflex coronary arterySevere coronary artery diseaseLeft circumflex coronary arteryGrowth factorCoronary arterial microvesselsCoronary microvascular reactivityProximal (<b>d</b>) LCX arteryEndothelium-dependent mechanismEndothelium-dependent relaxationCircumflex coronary arteryCollateral-dependent myocardiumCoronary artery diseaseTreatment of patientsGuanylate cyclase activators sodium nitroprussideChronic myocardial ischemiaAdenylate cyclase activator forskolinPeriadventitial administrationCyclase activator forskolinMicrovascular reactivity
1994
Pharmacological characterization of muscarinic receptors mediating acetylcholine-induced contraction and relaxation in rabbit intrapulmonary arteries.
Altiere R, Travis D, Roberts J, Thompson D. Pharmacological characterization of muscarinic receptors mediating acetylcholine-induced contraction and relaxation in rabbit intrapulmonary arteries. Journal Of Pharmacology And Experimental Therapeutics 1994, 270: 269-276. PMID: 8035325, DOI: 10.1016/s0022-3565(25)22363-1.Peer-Reviewed Original ResearchConceptsRelaxant responsesPA2 valuesContractile responsePulmonary arteryMuscarinic receptorsM1-selective antagonist pirenzepineEndothelium-dependent contractionsRabbit intrapulmonary arteriesEndothelium-dependent relaxationIsolated pulmonary arteriesM3-selective antagonistRabbit pulmonary arteryAcetylcholine-induced contractionsMuscarinic receptor subtypesN-methylpiperidine methiodideM2-selective antagonistSubtype-selective antagonistsNitric oxide synthaseInhibitor of cyclooxygenaseElevated toneAntagonist pirenzepineIntrapulmonary arteriesOxide synthaseReceptor subtypesPharmacological characterization
1990
L-Glutamine inhibits the release of endothelium-derived relaxing factor from the rabbit aorta
Swierkosz T, Mitchell J, Sessa W, Hecker M, Vane J. L-Glutamine inhibits the release of endothelium-derived relaxing factor from the rabbit aorta. Biochemical And Biophysical Research Communications 1990, 172: 143-148. PMID: 2222463, DOI: 10.1016/s0006-291x(05)80184-6.Peer-Reviewed Original ResearchConceptsRelease of EDRFRabbit aortic stripsAortic stripsRabbit aortaL-arginineL-ArgACh-induced relaxationEndothelium-dependent relaxationL-GlnL-Arg levelsIntact blood vesselsEDRF biosynthesisAortic tissueConsecutive infusionsEDRFL-glutamineAortaEndothelial cellsInitial equilibration periodBlood vesselsD-ArgInhibitory effectInfusionPresent studyAmino acid L-glutamine
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