Search results for "ENDOTHELIAL DYSFUNCTION"

showing 10 items of 287 documents

Uncoupling of Endothelial Nitric Oxide Synthase in Cardiovascular Disease and its Pharmacological Reversal

2010

Publisher Summary This chapter discusses the role of oxidative stress in vascular dysfunction and atherogenesis, and strategies for its prevention. Endothelial dysfunction and oxidative stress have been identified as a common denominator of many cardiovascular risk factors. They support pro-inflammatory, prothrombotic, proliferative, and vasoconstrictor mechanisms that are involved in the initiation, progression, and complications of atherosclerosis. The pathophysiologic causes of oxidative stress involve changes in a number of different enzyme systems. Increased production of ROS by uncoupled eNOS is likely to contribute significantly to vascular oxidative stress and endothelial dysfunctio…

chemistry.chemical_classificationReactive oxygen speciesmedicine.medical_specialtyNADPH oxidaseVascular smooth musclebiologymedicine.disease_causemedicine.diseaseNitric oxideSuperoxide dismutasechemistry.chemical_compoundEndocrinologychemistryInternal medicinebiology.proteinmedicineEndothelial dysfunctionPeroxynitriteOxidative stress
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Aerobic training and angiogenesis activation in patients with stable chronic heart failure: a preliminary report.

2013

The pathophysiology of chronic heart failure (CHF) involves multiple hystologic and molecular alterations. To determine the effects of physical training on circulating endothelial progenitor cells (EPCs), angiogenesis (angiogenin, angiopoietin-1 and -2, VEGF, Tie-2, SDF-1α) and inflammation (IL-6, CRP), we compared data obtained from 11 CHF pts before and after 3 months aerobic exercise training, to those from 10 non trained CHF pts (CHF-C group, age 64 + 2 years, NYHA 2). At the end of the study, EPCs count and AP-2 serum levels significantly increased in the CHF-TR group. These preliminary data suggest a significant effect of even a short program of physical training on angiogenic activat…

Malemedicine.medical_specialtyAngiogeninBrachial ArteryAngiogenesisHealth Toxicology and MutagenesisClinical BiochemistryNeovascularization PhysiologicCardiovascular disease growth factors/cytokines/inflammatory mediators sports science/exerciseInflammationPilot ProjectsBiochemistryNeovascularizationInternal medicinemedicineAerobic exerciseHumanscardiovascular diseasesProspective StudiesEndothelial dysfunctionAngiogenic ProteinsExerciseAgedHeart Failurebusiness.industryStem CellsEndothelial CellsStroke VolumeStroke volumeMiddle Agedmedicine.diseaseSettore MED/11 - Malattie Dell'Apparato CardiovascolareExercise TherapyVasodilationTreatment OutcomeHeart failureImmunologyChronic Diseasecardiovascular systemCardiologymedicine.symptombusinessBiomarkerscirculatory and respiratory physiologyBiomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals
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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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Diabetes and the COVID-19 Pandemic: How Insights from Recent Experience Might Guide Future Management

2020

medicine.medical_specialtyCoronavirus disease 2019 (COVID-19)Endocrinology Diabetes and MetabolismPneumonia ViralType 2 diabetesDiabetes ComplicationsDisease susceptibilityInsulin resistanceDiabetes mellitusPandemicmedicineInternal MedicineDiabetes MellitusHumansEndothelial dysfunctionIntensive care medicinePandemicsbusiness.industryCOVID-19medicine.diseaseObesityCommentarycardiovascular disease endothelial dysfunction insulin resistance obesity type 2 diabetes COVID-19 Coronavirus Infections Diabetes Complications Diabetes Mellitus Disease Susceptibility Humans Pandemics Pneumonia ViralDisease SusceptibilitybusinessCoronavirus Infections
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Manganese superoxide dismutase and aldehyde dehydrogenase deficiency increase mitochondrial oxidative stress and aggravate age-dependent vascular dys…

2008

AimsImbalance between pro- and antioxidant species (e.g. during aging) plays a crucial role for vascular function and is associated with oxidative gene regulation and modification. Vascular aging is associated with progressive deterioration of vascular homeostasis leading to reduced relaxation, hypertrophy, and a higher risk of thrombotic events. These effects can be explained by a reduction in free bioavailable nitric oxide that is inactivated by an age-dependent increase in superoxide formation. In the present study, mitochondria as a source of reactive oxygen species (ROS) and the contribution of manganese superoxide dismutase (MnSOD, SOD-2) and aldehyde dehydrogenase (ALDH-2) were inves…

Mitochondrial ROSMaleAgingPhysiologyVasodilator AgentsMitochondrionVascular dysfunctionmedicine.disease_causeMitochondria HeartMuscle Smooth Vascularchemistry.chemical_compoundMiceEndothelial dysfunctionAortachemistry.chemical_classificationMice KnockoutbiologySuperoxideAldehyde Dehydrogenase MitochondrialAge FactorsVasodilationBiochemistryCardiology and Cardiovascular MedicineMitochondrial aldehyde dehydrogenasemedicine.medical_specialty8-oxodGOxidative phosphorylationDNA MitochondrialSuperoxide dismutaseManganese superoxide dismutaseddc:570Physiology (medical)Internal medicinemedicineAnimalsReactive oxygen speciesDose-Response Relationship DrugSuperoxide DismutaseMitochondrial oxidative stressOriginal ArticlesAldehyde Dehydrogenasemedicine.diseaseMice Inbred C57BLOxidative StressEndocrinologychemistrybiology.proteinEndothelium VascularReactive Oxygen SpeciesOxidative stressDNA DamageCardiovascular research
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Subcortical ischaemic changes in young hypertensive patients: frequency, effect on cognitive performance and relationship with markers of endothelial…

2007

Information on subcortical ischaemic changes (SIC) in young hypertensive patients is scarce. We evaluated the frequency of SIC at magnetic resonance imaging (MRI), the possible effect on cognition of these patients, and the role of plasma markers known as indicators of endothelial and haemostatic activation. Inclusion criteria were age <or=54 years, hypertension for at least 2 years and absence of cerebrovascular disease or other conditions possibly related to SIC. Patients with SIC at MRI and two control groups (matched for age, sex and education) of hypertensive patients without SIC and non-hypertensive healthy subjects underwent an extensive neuropsychological examination and evaluation …

AdultMalemedicine.medical_specialtyPathologyEndotheliumNeuropsychological TestsBrain IschemiaCognitionstomatognathic systemVon Willebrand factorInternal medicinemedicineHumansAge FactorEffects of sleep deprivation on cognitive performanceEndothelial dysfunctionHemostasisbiologymedicine.diagnostic_testbusiness.industryAge FactorsNeuropsychologyBrainMagnetic resonance imagingBiomarkerHemostasiMiddle Agedmedicine.diseaseMagnetic Resonance ImagingBlood pressuremedicine.anatomical_structureNeurologyHemostasisHypertensionCardiologybiology.proteinFemaleEndothelium VascularNeurology (clinical)businessBiomarkersHumanEuropean Journal of Neurology
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Nitric oxide in the pathogenesis of vascular disease

2000

Nitric oxide (NO) is synthesized by at least three distinct isoforms of NO synthase (NOS). Their substrate and cofactor requirements are very similar. All three isoforms have some implications, physiological or pathophysiological, in the cardiovascular system. The endothelial NOS III is physiologically important for vascular homeostasis, keeping the vasculature dilated, protecting the intima from platelet aggregates and leukocyte adhesion, and preventing smooth muscle proliferation. Central and peripheral neuronal NOS I may also contribute to blood pressure regulation. Vascular disease associated with hypercholesterolaemia, diabetes, and hypertension is characterized by endothelial dysfunct…

medicine.medical_specialtyNitric Oxide Synthase Type IIIHypercholesterolemiaNitric Oxide Synthase Type IIVasodilationNitric OxideEndothelial NOSPathology and Forensic MedicineNitric oxidePathogenesischemistry.chemical_compoundInternal medicineHumansMedicineEndothelial dysfunctionbiologybusiness.industryVascular diseasemedicine.diseaseNitric oxide synthaseEndothelial stem cellOxidative StressEndocrinologychemistryCardiovascular DiseasesHypertensionbiology.proteinEndothelium VascularNitric Oxide SynthasebusinessDiabetic AngiopathiesThe Journal of Pathology
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Bazedoxifene increases the proliferation of human arterial endothelial cells but does not affect the expression of cyclins A, B, and D1 and of p27Kip1

2021

Endothelial dysfunction and denudation are considered a first step in atherosclerosis. Endothelial proliferation is key for cellular repair. The effect of bazedoxifene on the vascular endothelium h...

Endothelial proliferationEndotheliumChemistryEndocrinology Diabetes and MetabolismObstetrics and Gynecologymedicine.diseaseCell biologyBazedoxifeneVascular endotheliumEndocrinologymedicine.anatomical_structuremedicineEndothelial dysfunctionCyclinmedicine.drugGynecological Endocrinology
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Increased nitrotyrosine plasma levels in relation to systemic markers of inflammation and myeloperoxidase in chronic heart failure

2009

The presence of a reciprocal link between inflammation and oxidative/nitrosative stress has been postulated in chronic heart failure (CHF). We aimed to determine signs of nitrosative stress in serum/plasma of CHF patients. ELISA tests were used for quantification of serum/plasma levels of Nitrotyrosine (NT), H(2)O(2), total NO, nitrite (NO(2)(-)), myeloperoxidase (MPO), Tumor Necrosis Factor-alpha (TNFalpha) and pro-Brain Natriuretic Peptide (proBNP) in 66 CHF patients (9 in NYHA I, 34 NYHA II, 23 NYHA III) and in 14 age-matched healthy subjects. NT levels were higher in NYHA III CHF patients compared to NYHA II (p<0.05), NYHA I (p<0.03) and controls (p<0.02), whereas NO(2)(-) and total NO …

medicine.medical_specialtymedicine.drug_classInflammationSystemic inflammationGastroenterologyNITROSATIVE STRESSchemistry.chemical_compoundInternal medicineBlood plasmamedicineNatriuretic peptidecardiovascular diseasesOXIDATIVE STRESSEndothelial dysfunctionbiologybusiness.industryNitrotyrosinemedicine.diseasehumanitiesEndocrinologychemistryMyeloperoxidaseHeart failureENDOTHELIAL DYSFUNCTIONcardiovascular systembiology.proteinmedicine.symptomCardiology and Cardiovascular Medicinebusinesscirculatory and respiratory physiology
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AT1-receptor blockade by telmisartan upregulates GTP-cyclohydrolase I and protects eNOS in diabetic rats.

2008

Several enzymatic sources of reactive oxygen species (ROS) were described as potential reasons of eNOS uncoupling in diabetes mellitus. In the present study, we investigated the effects of AT1-receptor blockade with chronic telmisartan (25 mg/kg/day, 6.5 weeks) therapy on expression of the BH4-synthesizing enzyme GTP-cyclohydrolase I (GCH-I), eNOS uncoupling, and endothelial dysfunction in streptozotocin (STZ, 60 mg/kg iv, 7 weeks)-induced diabetes mellitus (type I). Telmisartan therapy did not modify blood glucose and body weight. Aortas from diabetic animals had vascular dysfunction as revealed by isometric tension studies (acetylcholine and nitroglycerin potency). Vascular and cardiac RO…

Blood GlucoseMalemedicine.medical_specialtyNitric Oxide Synthase Type IIImedicine.disease_causeBiochemistryBenzoatesReceptor Angiotensin Type 1chemistry.chemical_compoundEnosPhysiology (medical)Internal medicinemedicineDiabetes MellitusAnimalsTelmisartanEndothelial dysfunctionRats WistarXanthine oxidaseGTP CyclohydrolaseNADPH oxidasebiologySuperoxideBody WeightNADPH Oxidasesmedicine.diseaseStreptozotocinbiology.organism_classificationMitochondriaRatsUp-RegulationEnzyme ActivationOxidative StressEndocrinologychemistrybiology.proteinBenzimidazolesTelmisartanAngiotensin II Type 1 Receptor BlockersOxidative stressmedicine.drugFree radical biologymedicine
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