Search results for "endothelial dysfunction"

showing 10 items of 287 documents

Mitochondrial aldehyde dehydrogenase (ALDH-2)--maker of and marker for nitrate tolerance in response to nitroglycerin treatment.

2008

The hemodynamic and anti-ischemic effects of nitroglycerin (GTN) are rapidly blunted as a result of the development of nitrate tolerance. Long-term nitrate treatment also is associated with decreased vascular responsiveness caused by changes in intrinsic mechanisms of the tolerant vasculature itself. According to the oxidative stress concept, increased vascular superoxide and peroxynitrite production as well as an increased sensitivity to vasoconstrictors secondary to activation of protein kinase C as well as vascular NADPH oxidases contribute to the development of tolerance. Recent experimental work has defined new tolerance mechanisms, including inhibition of the enzyme that bioactivates …

Aldehyde dehydrogenasePharmacologyToxicologymedicine.disease_causeProstacyclin synthasechemistry.chemical_compoundNitroglycerinDrug tolerancemedicineHumansEndothelial dysfunctionchemistry.chemical_classificationReactive oxygen speciesNitratesbiologyAldehyde Dehydrogenase MitochondrialGeneral MedicineDrug ToleranceAldehyde Dehydrogenasemedicine.diseaseMitochondriaOxidative StresschemistryBiochemistrycardiovascular systembiology.proteinSoluble guanylyl cyclasePeroxynitriteOxidative stresscirculatory and respiratory physiologyChemico-biological interactions
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Exploiting the Pleiotropic Antioxidant Effects of Established Drugs in Cardiovascular Disease.

2015

Cardiovascular disease is a leading cause of death and reduced quality of life worldwide. Arterial vessels are a primary target for endothelial dysfunction and atherosclerosis, which is accompanied or even driven by increased oxidative stress. Recent research in this field identified different sources of reactive oxygen and nitrogen species contributing to the pathogenesis of endothelial dysfunction. According to lessons from the past, improvement of endothelial function and prevention of cardiovascular disease by systemic, unspecific, oral antioxidant therapy are obviously too simplistic an approach. Source- and cell organelle-specific antioxidants as well as activators of intrinsic antiox…

Antioxidantmedicine.medical_treatmentGlucagon-Like PeptidesInflammationDiseaseReviewBiologymedicine.disease_causeCatalysisAntioxidantsendothelial dysfunctionInorganic ChemistryPathogenesislcsh:Chemistrycardiovascular diseasemedicineAnimalsHumansImmunologic FactorsPhysical and Theoretical ChemistryEndothelial dysfunctionMolecular Biologylcsh:QH301-705.5Spectroscopyglucagon-like peptide analogsCause of deathInflammationOrganic ChemistryGeneral Medicinemedicine.diseaseComputer Science ApplicationsClinical trialOxidative Stresslcsh:Biology (General)lcsh:QD1-999Cardiovascular DiseasesImmunologyEndothelium Vascularmedicine.symptomdipeptidyl peptidase-4 inhibitorsOxidative stressInternational journal of molecular sciences
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Short-term e-cigarette vapour exposure causes vascular oxidative stress and dysfunction: evidence for a close connection to brain damage and a key ro…

2019

Abstract Aims Electronic (e)-cigarettes have been marketed as a ‘healthy’ alternative to traditional combustible cigarettes and as an effective method of smoking cessation. There are, however, a paucity of data to support these claims. In fact, e-cigarettes are implicated in endothelial dysfunction and oxidative stress in the vasculature and the lungs. The mechanisms underlying these side effects remain unclear. Here, we investigated the effects of e-cigarette vapour on vascular function in smokers and experimental animals to determine the underlying mechanisms. Methods and results Acute e-cigarette smoking produced a marked impairment of endothelial function in chronic smokers determined b…

Behavioural risk factorInflammationElectronic Nicotine Delivery Systems030204 cardiovascular system & hematologyPharmacologymedicine.disease_causeVascular MedicineLifestyle drugNicotineLipid peroxidationMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBasic ScienceAnimalsHumansMedicineEndothelial dysfunction030212 general & internal medicineEndothelial dysfunctionMacitentanNADPH oxidasebiologybusiness.industryBrainNADPH Oxidasesmedicine.diseaseE-cigarette vapourEditor's ChoiceLeukemia Myeloid AcuteOxidative Stressmedicine.anatomical_structurechemistryE-Cigarette VaporNADPH Oxidase 2Neoplastic Stem Cellsbiology.proteinmedicine.symptomCardiology and Cardiovascular MedicinebusinessOxidative stressmedicine.drugBlood vesselEuropean Heart Journal
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GLP-1 receptor agonists and reduction of cardiometabolic risk: Potential underlying mechanisms

2018

Type 2 diabetes mellitus (T2DM) is a metabolic condition with an elevated impact on cardiovascular (CV) risk. The innovative therapeutic approaches for T2DM - incretin-based therapies (IBTs), including glucagon-like peptide 1 (GLP-1) receptor agonists, have become popular and more widely used in recent years. The available scientific data from clinical studies and clinical practice highlights their beyond glucose-lowering effects, which is achieved without any increase in hypoglycaemia. The former effects include reduction in body weight, lipids, blood pressure, inflammatory markers, oxidative stress, endothelial dysfunction, and subclinical atherosclerosis, thus reducing and potentially pr…

Blood GlucoseCardiometabolic parameterGlucagon-Like PeptidesIncretin030209 endocrinology & metabolism030204 cardiovascular system & hematologyBioinformaticsIncretinsGlucagon-Like Peptide-1 Receptor03 medical and health sciences0302 clinical medicineDiabetes mellitusmedicineHumansHypoglycemic AgentsEndothelial dysfunctionMolecular BiologyGlucagon-like peptide 1 receptorLiraglutidebusiness.industryType 2 Diabetes MellitusLiraglutideCardiovascular riskmedicine.diseasePlaque AtheroscleroticType 2 diabetes mellituBlood pressureDiabetes Mellitus Type 2Cardiovascular DiseasesMetabolic control analysisGlucagon-like peptide 1 receptor agonistMolecular Medicinebusinessmedicine.drugBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Chronic peroxisome proliferator-activated receptorβ/δ agonist GW0742 prevents hypertension, vascular inflammatory and oxidative status, and endotheli…

2015

Endothelial dysfunction plays a key role in obesity-induced risk of cardiovascular disease. The aim of the present study was to analyze the effect of chronic peroxisome proliferator-activated receptor (PPAR)β/δ agonist GW0742 treatment on endothelial function in obese mice fed a high-fat diet (HFD).Five-week-old male mice were allocated to one of the following groups: control, control-treated (GW0742, 3 mg/kg per day, by oral gavage), HFD, HFD + GW0742, HFD + GSK0660 (1 mg/kg/day, intraperitoneal) or HFD-GW0742-GSK0660 and followed for 11 or 13 weeks. GW0742 administration to mice fed HFD prevented the gain of body weight, heart and kidney hypertrophy, and fat accumulation. The increase in …

Blood GlucoseMaleAgonistmedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumPhysiologymedicine.drug_classCaveolin 1Peroxisome proliferator-activated receptorThiophenesDiet High-FatGW0742MiceInsulin resistanceInternal medicineInternal MedicinemedicineAnimalsObesityPPAR deltaSulfonesEndothelial dysfunctionReceptorPPAR-betaAortachemistry.chemical_classificationInterleukin-6Tumor Necrosis Factor-alphabusiness.industryGlucose Tolerance TestPeroxisomemedicine.diseaseToll-Like Receptor 4VasodilationThiazolesEndocrinologymedicine.anatomical_structureAdipose TissuechemistryHypertensionAdiponectinEndothelium VascularInsulin ResistanceReactive Oxygen SpeciesCardiology and Cardiovascular MedicinebusinessJournal of Hypertension
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Effects of oral niacin on endothelial dysfunction in patients with coronary artery disease: Results of the randomized, double-blind, placebo-controll…

2009

High-density-lipoproteins-cholesterol (HDL-C) is invertedly related to the incidence of cardiovascular events. Recent studies suggest that HDL-C directly improves endothelial function. Nicotinic acid (niacin) effectively raises serum HDL-C. We therefore hypothesized that treatment with niacin improves endothelial dysfunction in patients with coronary artery disease (CAD). One hundred seven patients with CAD were randomly assigned to double-blinded treatment for 12 weeks with extended-release (ER)-niacin 1000 mg/day (N) or placebo (C), respectively. Flow-mediated dilation (FMD) of the brachial artery, nitroglycerin-mediated endothelium-independent dilation (NMD) and serum lipid concentration…

Blood GlucoseMalemedicine.medical_specialtyBrachial ArteryVasodilator AgentsAdministration OralCoronary Artery DiseasePlaceboNiacinGastroenterologyCoronary artery diseaseNitroglycerinchemistry.chemical_compoundHigh-density lipoproteinDouble-Blind MethodInternal medicinemedicine.arterymedicineHumansProspective StudiesPhosphorylationEndothelial dysfunctionBrachial arteryTriglyceridesAgedUltrasonographyVascular diseasebusiness.industryCholesterol HDLMicrofilament Proteinsnutritional and metabolic diseasesCholesterol LDLMiddle AgedPhosphoproteinsmedicine.diseaseVasodilationB vitaminsTreatment OutcomeEndocrinologychemistryDelayed-Action PreparationsFemalelipids (amino acids peptides and proteins)Endothelium VascularCardiology and Cardiovascular MedicinebusinessCell Adhesion MoleculesBiomarkersNiacinAtherosclerosis
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Vascular Dysfunction in Streptozotocin-Induced Experimental Diabetes Strictly Depends on Insulin Deficiency

2010

<i>Objective:</i> In previous studies we and others have shown that streptozotocin (STZ)-induced diabetes in rats is associated with vascular oxidative stress and dysfunction. In the present study, we sought to determine whether vascular dysfunction and oxidative stress strictly depend on insulin deficiency. <i>Methods:</i> The effects of insulin (2.5 U/day s.c., 2 weeks) therapy on vascular disorders in STZ-induced (60 mg/kg i.v., 8 weeks) diabetes mellitus (type I) were studied in Wistar rats. The contribution of NADPH oxidase to overall oxidative stress was investigated by in vivo (30 mg/kg/day s.c., 4 days) and in vitro treatment with apocynin. <i>Results:&…

Blood GlucoseMalemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumPhysiologymedicine.medical_treatmentmedicine.disease_causeStreptozocinDiabetes Mellitus Experimentalchemistry.chemical_compoundInternal medicineDiabetes mellitusmedicineAnimalsInsulinRats WistarEndothelial dysfunctionNADPH oxidasebiologybusiness.industryMyocardiumInsulinAcetophenonesNADPH OxidasesStreptozotocinmedicine.diseaseRatsOxidative StressNG-Nitroarginine Methyl EsterEndocrinologymedicine.anatomical_structurechemistryApocyninbiology.proteinEndothelium VascularCardiology and Cardiovascular MedicinebusinessDiabetic AngiopathiesOxidative stressmedicine.drugJournal of Vascular Research
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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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Involvement of prostacyclin and potassium channels in the diabetes-induced hyporeactivity of the rabbit carotid artery to B-type natriuretic peptide

2012

The relation between diabetes and stroke is bidirectional: diabetes is an important risk factor for ischemic stroke, and acute stroke frequently induces hyperglycemia. On the other hand, plasma B-type natriuretic peptide (BNP) levels are raised in diabetes and stroke. The purpose was to study how alloxan-induced diabetes might modify the effects of BNP in rabbit carotid arteries and the mechanisms involved in such actions. To do this, isometric tension in isolated rabbit carotid artery was recorded and prostanoids release and plasma NT-proBNP were measured by enzyme immunoassay. BNP induced a relaxation of phenylephrine-precontracted carotid arteries, and this relaxation was lower in diabet…

Blood GlucoseMalemedicine.medical_specialtyPotassium ChannelsEndotheliummedicine.drug_classProstacyclinNitric OxideGlibenclamideThromboxane A2chemistry.chemical_compoundDiabetes mellitusInternal medicineNatriuretic Peptide BrainDiabetes MellitusmedicineNatriuretic peptideAnimalscardiovascular diseasesEndothelial dysfunctionStrokePharmacologyDose-Response Relationship Drugbusiness.industryBody Weightmedicine.diseaseEpoprostenolPeptide FragmentsCarotid Arteriesmedicine.anatomical_structureEndocrinologychemistryPotassiumcardiovascular systemRabbitsbusinessReceptors Atrial Natriuretic Factorhormones hormone substitutes and hormone antagonistsmedicine.drugEuropean Journal of Pharmacology
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Vascular Dysfunction in Experimental Diabetes Is Improved by Pentaerithrityl Tetranitrate but Not Isosorbide-5-Mononitrate Therapy

2011

OBJECTIVE Diabetes is associated with vascular oxidative stress, activation of NADPH oxidase, and uncoupling of nitric oxide (NO) synthase (endothelial NO synthase [eNOS]). Pentaerithrityl tetranitrate (PETN) is an organic nitrate with potent antioxidant properties via induction of heme oxygenase-1 (HO-1). We tested whether treatment with PETN improves vascular dysfunction in the setting of experimental diabetes. RESEARCH DESIGN AND METHODS After induction of hyperglycemia by streptozotocin (STZ) injection (60 mg/kg i.v.), PETN (15 mg/kg/day p.o.) or isosorbide-5-mononitrate (ISMN; 75 mg/kg/day p.o.) was fed to Wistar rats for 7 weeks. Oxidative stress was assessed by optical methods and o…

Blood GlucoseMalemedicine.medical_specialtyXanthine OxidaseEndocrinology Diabetes and MetabolismVasodilator AgentsOxidative phosphorylationIsosorbide Dinitratemedicine.disease_causeWeight GainNitric oxideDiabetes Mellitus Experimentalchemistry.chemical_compoundEnosInternal medicineInternal MedicinemedicineAnimalsPentaerythritol TetranitrateGene SilencingEndothelial dysfunctionRats WistarXanthine oxidaseGTP CyclohydrolaseNADPH oxidasebiologyNADPH Oxidasesmedicine.diseasebiology.organism_classificationStreptozotocinPharmacology and TherapeuticsRatsOxidative StressEndocrinologychemistryVasoconstrictionbiology.proteinEndothelium VascularReactive Oxygen SpeciesOxidative stressHeme Oxygenase-1medicine.drugDiabetes
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