Search results for "endothelial dysfunction"

showing 10 items of 287 documents

Chronic exercise impairs nitric oxide pathway in rabbit carotid and femoral arteries

2018

KEY POINTS: Some of the beneficial effects of exercise in preventing vascular related diseases are mediated by the enhancement of endothelial function where the role of nitric oxide (NO) is well documented, although the relevance of calcium activated potassium channels is not fully understood. The impact of oxidative stress induced by training on endothelial function remains to be clarified. By evaluating different endothelial vasodilator pathways on two vascular beds in a rabbit model of chronic exercise, we found a decreased NO bioavailability and endothelial nitric oxide synthase expression in both carotid and femoral arteries. Physical training induced carotid endothelial dysfunction as…

Male0301 basic medicinemedicine.medical_specialtyPhysiologyVasodilationFemoral artery030204 cardiovascular system & hematologyNitric OxideApaminNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEnosPhysical Conditioning AnimalInternal medicinemedicine.arterymedicineAnimalsLarge-Conductance Calcium-Activated Potassium ChannelsEndothelial dysfunctionExercisebiologybiology.organism_classificationmedicine.diseaseCalcium-activated potassium channelFemoral ArteryOxidative StressCarotid Arteries030104 developmental biologyEndocrinologychemistryNitric Oxide PathwayEndothelium VascularRabbitsThe Journal of Physiology
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Glutathione Peroxidase-1 Deficiency Potentiates Dysregulatory Modifications of Endothelial Nitric Oxide Synthase and Vascular Dysfunction in Aging

2014

Recently, we demonstrated that gene ablation of mitochondrial manganese superoxide dismutase and aldehyde dehydrogenase-2 markedly contributed to age-related vascular dysfunction and mitochondrial oxidative stress. The present study has sought to investigate the extent of vascular dysfunction and oxidant formation in glutathione peroxidase-1–deficient ( GPx-1 −/− ) mice during the aging process with special emphasis on dysregulation (uncoupling) of the endothelial NO synthase. GPx-1 −/− mice on a C57 black 6 (C57BL/6) background at 2, 6, and 12 months of age were used. Vascular function was significantly impaired in 12-month-old GPx-1 −/− -mice as compared with age-matched controls. Oxidan…

MaleAgingmedicine.medical_specialtyGPX1Nitric Oxide Synthase Type IIIBiologymedicine.disease_causeMicechemistry.chemical_compoundGlutathione Peroxidase GPX1Internal medicineLeukocytesInternal MedicinemedicineAnimalsHumansPhosphorylationEndothelial dysfunctionProtein kinase ACells CulturedAgedMice Knockoutchemistry.chemical_classificationGlutathione PeroxidaseGlutathione peroxidaseEndothelial CellsNitric Oxide Synthase Type IIIGlutathioneOxidantsmedicine.diseaseMice Inbred C57BLOxidative StressEndocrinologychemistryImmunologyPhosphorylationEndothelium VascularOxidative stressHypertension
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Inflammatory activation and endothelial dysfunction markers in patients with permanent atrial fibrillation: A cross-sectional study

2020

In recent years a growing body of evidence supported the role of inflammation in the initiation, maintenance and outcome of atrial fibrillation (AF). Nevertheless, despite a large amount of information, whether AF or the underlying structural heart disease (SHD) is the cause of the inflammatory process is still under debate. We, therefore, sought to determine if the inflammatory process reflect an underlying disease or the arrhythmia 'per se'. We evaluated plasma levels of soluble Interleukin 2 Receptor Alpha (sIL-2Rα), TNF-α and IL-18 in 100 consecutive patients with permanent AF, (43 with a SHD and 57 without a SHD) compared to 121 age and sex-matched controls which had normal sinus rhyth…

MaleAgingmedicine.medical_specialtyHeart diseaseAlpha (ethology)InflammationDiseaseSystemic inflammationendothelial dysfunctionInternal medicineAtrial FibrillationmedicineHumansEndothelial dysfunctionReactive hyperemiaAgedAged 80 and overInflammationTumor Necrosis Factor-alphabusiness.industryInterleukin-18Interleukin-2 Receptor alpha SubunitAtrial fibrillationAtrial fibrillation Cytokines Endothelial dysfunction Inflammation Structural heart diseaseCell BiologyMiddle Agedmedicine.diseasestructural heart diseasecytokinesCross-Sectional StudiesLogistic ModelsROC CurveCase-Control StudiesCardiologyFemaleEndothelium Vascularmedicine.symptombusinessBiomarkersResearch Paper
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Short-Term Effects of a Combined Nutraceutical on Lipid Level, Fatty Liver Biomarkers, Hemodynamic Parameters, and Estimated Cardiovascular Disease R…

2017

Introduction: There is a growing interest in nutraceuticals improving cardiovascular risk factor levels and related organ damage. Methods: This double-blind, placebo-controlled randomized clinical trial aims to compare the effect of a combined nutraceutical containing red yeast rice (10 mg), phytosterols (800 mg), and l-tyrosol (5 mg) on lipid profile, blood pressure, endothelial function, and arterial stiffness in a group of 60 patients with polygenic hypercholesterolemia resistant to Mediterranean diet. Results: After 8 weeks of treatment, when compared to the placebo group, the active treated patients experienced a more favorable percentage change in total cholesterol (−16.3% vs 9.9…

MaleBlood Pressure030204 cardiovascular system & hematologyGastroenterologychemistry.chemical_compoundDietary supplement0302 clinical medicineRisk FactorsPhytosterolPharmacology (medical)030212 general & internal medicineEndothelial dysfunctionOriginal ResearchFramingham Risk Scoremedicine.diagnostic_testAnticholesteremic AgentsFatty liverPhytosterolsGeneral MedicineMiddle AgedDietary supplementsCholesterolBiochemistryCardiovascular DiseasesFemaleNutraceuticalsNutraceuticalAdultmedicine.medical_specialtyl-TyrosolHypercholesterolemiaPlacebo03 medical and health sciencesDouble-Blind MethodInternal medicinemedicineHumansRisk factorBiological ProductsCholesterolbusiness.industryHemodynamicsmedicine.diseaseCardiovascular disease riskBlood pressurechemistryRed yeast riceArterial stiffnessLipid profilebusinessBiomarkers
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Molecular basis of endothelial dysfunction in sepsis.

2003

Sepsis is one of the major causes of mortality in critically ill patients and develops as a result of the host response to infection. A complex network of events is set into motion in the body by the infection and results in the pathogenesis of sepsis. This review article focuses on the molecular mechanisms and components involved in the pathogenesis of sepsis with a major emphasis on the endothelium. This includes sepsis-inducing bacterial components (e.g. endotoxins), cellular targets of these molecules and their responses, host reactions, intracellular and cytokine networks, individual susceptibility and new therapeutic targets in sepsis treatment.

MaleEndotheliumPhysiologymedicine.medical_treatmentReceptors Cell SurfaceBiologyNitric OxidePathogenesisSepsisPhysiology (medical)SepsismedicineHumansEndothelial dysfunctionHypoxiaMembrane GlycoproteinsToll-Like ReceptorsEndothelial Cellsmedicine.diseaseReview articleBacterial adhesinEndotoxinsmedicine.anatomical_structureCytokineImmunologyMutationCytokinesFemaleDisease SusceptibilityEndothelium VascularCardiology and Cardiovascular MedicineReactive Oxygen SpeciesCell Adhesion MoleculesIntracellularInterleukin-1Cardiovascular research
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Influence of experimental diabetes on regulatory mechanisms of vascular response of rabbit carotid artery to acetylcholine

2000

Summary The purpose of this study was to analyse the influence of experimental diabetes on vascular response of rabbit carotid artery to acetylcholine (Ach). We compared the Ach-induced relaxant response of isolated arterial segments obtained from both control and diabetic animals. To assess the influence of the endothelium, this cell layer was mechanically removed in some of the arterial segments (“rubbed arteries”) from each experimental group. Ach induced a concentration-related endothelium-mediated relaxation of carotid artery from control rabbits that was significantly higher with respect to that obtained in diabetic animals. Pre-treatment with NG-nitro-L-arginine (L-NA) induced a conc…

MaleGene isoformmedicine.medical_specialtyEndotheliumVasodilator AgentsIndomethacinProstacyclinGuanidinesNitroarginineGeneral Biochemistry Genetics and Molecular BiologyDiabetes Mellitus ExperimentalNitric oxidechemistry.chemical_compoundInternal medicineDiabetes mellitusAlloxanmedicineAnimalsEnzyme InhibitorsGeneral Pharmacology Toxicology and PharmaceuticsEndothelial dysfunctionbusiness.industryAnti-Inflammatory Agents Non-SteroidalGeneral Medicinemedicine.diseaseAcetylcholineCarotid ArteriesEndocrinologymedicine.anatomical_structurechemistryArachidonic acidEndothelium VascularRabbitsbusinessAcetylcholinemedicine.drugLife Sciences
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An Expert Opinion From the European Society of Hypertension–European Union Geriatric Medicine Society Working Group on the Management of Hypertension…

2016

Two years after the publication of the 2013 guidelines for the management of arterial hypertension of the European Society of Hypertension (ESH) and the European Society of Cardiology (ESC),1 the ESH and the European Union Geriatric Medicine Society have created a common working group to examine the management of hypertensive subjects aged >80 years. The general term hypertension in the elderly is not sufficiently accurate because it mixes younger old patients (60–70 years) with the oldest old. Our group believes that the management of hypertension in individuals aged ≥80 years should be specifically addressed. Although arbitrary, this cutoff value identifies a population that is expanding …

MaleGerontologyBLOOD-PRESSUREL-ARGININE TRANSPORTFAT-FED RABBITS030204 cardiovascular system & hematologySeverity of Illness IndexSYMPATHETIC-NERVE ACTIVITY0302 clinical medicine80 and overPerindopril030212 general & internal medicineDisease management (health)Societies MedicalComputingMilieux_MISCELLANEOUSMETABOLIC SYNDROMEmedia_commonAged 80 and overGeriatricseducation.field_of_study[SDV.MHEP] Life Sciences [q-bio]/Human health and pathology[SDV.MHEP.GEG] Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontology[SDV.MHEP.GEG]Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontologyIndapamideDisease ManagementPrognosis[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system3. Good healthAntihypertensive AgentTreatment OutcomeHypertensionPractice Guidelines as TopicFemaleSurvival AnalysiHumanmedicine.drugANGIOTENSIN-CONVERTING ENZYMEmedicine.medical_specialtyPrognosiFrail ElderlyeducationPopulationRisk Assessment03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemMedicalInternal MedicinemedicineHumansmedia_common.cataloged_instanceEuropean UnionNITRIC-OXIDE SYNTHASEEuropean unioneducationREDUCES OXIDATIVE STRESSExpert TestimonyGeriatric AssessmentAntihypertensive AgentsAgedAged; Aged 80 and over; Antihypertensive Agents; Blood Pressure Determination; Disease Management; European Union; Expert Testimony; Female; Frail Elderly; Geriatric Assessment; Geriatrics; Humans; Hypertension; Male; Prognosis; Risk Assessment; Severity of Illness Index; Societies Medical; Survival Analysis; Treatment Outcome; Practice Guidelines as Topic; Internal Medicinebusiness.industryBlood Pressure DeterminationSurvival AnalysisBlood pressureOBESITY-INDUCED HYPERTENSIONGeriatrics3121 General medicine internal medicine and other clinical medicineENDOTHELIAL DYSFUNCTIONLife expectancySocietiesbusinessGeriatric[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyHypertension
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Effect of soluble guanylyl cyclase activator and stimulator therapy on nitroglycerin-induced nitrate tolerance in rats

2015

Chronic nitroglycerin (GTN) anti-ischemic therapy induces side effects such as nitrate tolerance and endothelial dysfunction. Both phenomena could be based on a desensitization/oxidation of the soluble guanylyl cyclase (sGC). Therefore, the present study aims at investigating the effects of the therapy with the sGC activator BAY 60-2770 and the sGC stimulator BAY 41-8543 on side effects induced by chronic nitroglycerin treatment. Male Wistar rats were treated with nitroglycerin (100mg/kg/d for 3.5days, s.c. in ethanol) and BAY 60-2770 (0.5 or 2.5mg/kg/d) or BAY 41-8543 (1 and 5mg/kg/d) for 6days. Therapy with BAY 60-2770 but not with BAY 41-8543 improved nitroglycerin-triggered endothelial …

MaleHydrocarbons FluorinatedPhysiologyMorpholinesReceptors Cytoplasmic and NuclearVasodilationStimulationPharmacologymedicine.disease_causeBenzoatesNitric oxideNitroglycerinchemistry.chemical_compoundOrgan Culture TechniquesSoluble Guanylyl CyclasemedicineAnimalsPharmacology (medical)Rats WistarEndothelial dysfunctionAortaWhole bloodPharmacologyNitratesActivator (genetics)business.industryNitrotyrosineBiphenyl Compoundsmedicine.diseaseRatsBiphenyl compoundEnzyme ActivationOxidative StressPyrimidineschemistryGuanylate CyclaseMeeting Abstractcardiovascular systemMolecular MedicineSoluble guanylyl cyclasebusinessOxidative stressBMC Pharmacology and Toxicology
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Nitroglycerin-induced endothelial dysfunction and tolerance involve adverse phosphorylation and S-glutathionylation of endothelial nitric oxide synth…

2011

Continuous administration of nitroglycerin (GTN) causes tolerance and endothelial dysfunction by inducing reactive oxygen species (ROS) production from various enzymatic sources, such as mitochondria, NADPH oxidase, and an uncoupled endothelial nitric oxide synthase (eNOS). In the present study, we tested the effects of type 1 angiotensin (AT(1))-receptor blockade with telmisartan on GTN-induced endothelial dysfunction in particular on eNOS phosphorylation and S-glutathionylation sites and the eNOS cofactor synthesizing enzyme GTP-cyclohydrolase I.Wistar rats were treated with telmisartan (2.7 or 8 mg/kg per day PO for 10 days) and with GTN (50 mg/kg per day SC for 3 days). Aortic eNOS phos…

MaleNitric Oxide Synthase Type IIIPhysiologyVasodilator AgentsPharmacologyBenzoatesCell LineNitroglycerinmedicineAnimalsHumansTelmisartanEnzyme InhibitorsPhosphorylationRats WistarS-GlutathionylationEndothelial dysfunctionGTP CyclohydrolaseBeneficial effectsNitroglycerinPharmacologyAngiotensin II receptor type 1Dose-Response Relationship DrugEndothelial nitric oxide synthaseChemistryEndothelial CellsDrug ToleranceAldehyde Dehydrogenasemedicine.diseaseGlutathioneMitochondriaRatsVasodilationOxidative StressTetrahydrofolate DehydrogenaseMolecular MedicinePhosphorylationBenzimidazolesEndothelium VascularTelmisartanReactive Oxygen SpeciesAngiotensin II Type 1 Receptor BlockersProtein Processing Post-Translationalmedicine.drugVascular Pharmacology
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Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX 3 CL1) Expression by Angiotensin-II

2012

Objective— Angiotensin-II (Ang-II) promotes the interaction of mononuclear cells with arterioles and neutrophils with postcapillary venules. To investigate the mechanisms underlying this dissimilar response, the involvement of fractalkine (CX 3 CL1) was explored. Methods and Results— Enhanced CX 3 CL1 expression was detected in both cremasteric arterioles and postcapillary venules 24 hours after Ang-II intrascrotal injection. Arteriolar leukocyte adhesion was the unique parameter significantly reduced (83%) in animals lacking CX 3 CL1 receptor (CX 3 CR1). Human umbilical arterial and venous endothelial cell stimulation with 1 μmol/L Ang-II increased CX 3 CL1 expression, yet neutralization …

MalePathologyTime Factorsp38 Mitogen-Activated Protein KinasesMiceVenulesLeukocytesEndothelial dysfunctionExtracellular Signal-Regulated MAP KinasesReceptorCells CulturedMice KnockoutMembrane GlycoproteinsAngiotensin IINF-kappa BArteriesEndothelial stem cellArteriolesNADPH Oxidase 5NADPH Oxidase 4NADPH Oxidase 2FemaleRNA InterferenceReceptors ChemokineTumor necrosis factor alphaCardiology and Cardiovascular MedicineSignal Transductionmedicine.medical_specialtyCX3C Chemokine Receptor 1BiologyTransfectionPeripheral blood mononuclear cellLosartanVeinsInterferon-gammaApolipoproteins EDownregulation and upregulationInternal medicineCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansLeukocyte RollingCX3CL1Chemokine CX3CL1Tumor Necrosis Factor-alphaEndothelial CellsMembrane ProteinsNADPH OxidasesAtherosclerosismedicine.diseaseAngiotensin IIMice Inbred C57BLDisease Models AnimalEndocrinologyAngiotensin II Type 1 Receptor BlockersArteriosclerosis, Thrombosis, and Vascular Biology
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