Search results for "endothelial dysfunction"

showing 10 items of 287 documents

The impact of aircraft noise on vascular and cardiac function in relation to noise event number: a randomized trial

2020

Abstract Aims Nighttime aircraft noise exposure has been associated with increased risk of hypertension and myocardial infarction, mechanistically linked to sleep disturbance, stress, and endothelial dysfunction. It is unclear, whether the most widely used metric to determine noise exposure, equivalent continuous sound level (Leq), is an adequate indicator of the cardiovascular impact induced by different noise patterns. Methods and results In a randomized crossover study, we exposed 70 individuals with established cardiovascular disease or increased cardiovascular risk to two aircraft noise scenarios and one control scenario. Polygraphic recordings, echocardiography, and flow-mediated dila…

MaleTime FactorsAircraft noiseAircraftBrachial ArteryPhysiologyDenmark030204 cardiovascular system & hematologyVentricular Function Leftlaw.invention0302 clinical medicineRandomized controlled triallawDiastoleAcademicSubjects/MED00200030212 general & internal medicineMyocardial infarctionEndothelial dysfunctionAircraft noise exposureSleep disorderCross-Over StudiesMiddle AgedEchocardiography DopplerIrritable MoodFlow-mediated dilationVasodilationEnvironmental healthCardiovascular DiseasesNoise TransportationCardiologyDisease ProgressionFemaleCardiology and Cardiovascular MedicineCardiac function curvemedicine.medical_specialtyRisk in Cardiovascular DiseaseDiastoleSleep disturbance03 medical and health sciencesDouble-Blind MethodPhysiology (medical)Internal medicinemedicinePressureHumansAgedbusiness.industryCardiac functionStroke VolumeOriginal ArticlesVascular functionmedicine.diseaseCrossover studybusinessCardiovascular Research
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Nitric oxide synthase inhibition and oxidative stress in cardiovascular diseases: Possible therapeutic targets?

2013

International audience; Nitric oxide (• NO) is synthetized enzymatically from L-arginine (L-Arg) by three NO synthase isoforms, iNOS, eNOS and nNOS. The synthesis of NO is selectively inhibited by guanidino-substituted analogs of L-Arg or methylarginines such as asymmetric dimethylarginine (ADMA), which results from protein degradation in cells. Many disease states, including cardiovascular diseases and diabetes, are associated with increased plasma levels of ADMA. The N-terminal catalytic domain of these NOS isoforms binds the heme prosthetic group as well as the redox cofactor, tetrahydrobiopterin (BH 4) associated with a regulatory protein, calmodulin (CaM). The enzymatic activity of NOS…

NO inhibitorsfree radicals030204 cardiovascular system & hematologyProtein degradationPharmacologyNitric OxideNitric oxide03 medical and health scienceschemistry.chemical_compoundBH 40302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemcardiovascular diseaseEnosmedicineAnimalsHumansPharmacology (medical)Enzyme InhibitorsEndothelial dysfunctionReactive nitrogen species030304 developmental biologyPharmacologyNO synthases0303 health sciencesbiologyTetrahydrobiopterinbiology.organism_classificationmedicine.disease[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system3. Good healthADMANitric oxide synthaseOxidative StresschemistryBiochemistryCardiovascular Diseasesbiology.proteinNitric Oxide SynthaseAsymmetric dimethylargininemedicine.drugPharmacology & Therapeutics
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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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Dietary salt promotes ischemic brain injury and is associated with parenchymal migrasome formation

2018

Sodium chloride promotes vascular fibrosis, arterial hypertension, pro-inflammatory immune cell polarization and endothelial dysfunction, all of which might influence outcomes following stroke. But despite enormous translational relevance, the functional importance of sodium chloride in the pathophysiology of acute ischemic stroke is still unclear. In the current study, we show that high-salt diet leads to significantly worse functional outcomes, increased infarct volumes, and a loss of astrocytes and cortical neurons in acute ischemic stroke. While analyzing the underlying pathologic processes, we identified the migrasome as a novel, sodium chloride-driven pathomechanism in acute ischemic …

0301 basic medicineMalePathologyMacroglial CellsSodium ChlorideVascular MedicineBrain IschemiaMice0302 clinical medicineCytosolAnimal CellsMedicine and Health SciencesMedicineEndothelial dysfunctionStrokeNeuronsCerebral CortexCerebral IschemiaMultidisciplinaryQRPathophysiologyStrokeChemistryNeurologyPhysical SciencesImmunohistochemistryMedicineCellular Structures and OrganellesCellular TypesIntracellularResearch Articlemedicine.medical_specialtyScienceCerebrovascular DiseasesGlial Cells03 medical and health sciencesImmune systemIn vivoParenchymaAnimalscardiovascular diseasesVesiclesSodium Chloride DietaryMicroglial CellsNutritionIschemic StrokeOrganellesbusiness.industryChemical CompoundsBiology and Life SciencesCell Biologymedicine.diseaseDiet030104 developmental biologyCellular NeuroscienceAstrocytesBrain InjuriesSaltsbusiness030217 neurology & neurosurgeryNeurosciencePLoS ONE
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Is At Least One Vitamin Helping Our Vasculature?

2014

See related article, pp 1290–1298 Cardiovascular risk factors such as diabetes mellitus, arterial hypertension, chronic smoking, and hypercholesterolemia are cardiovascular risk factors known to be associated with endothelial dysfunction, a condition that may predict long-term progression of atherosclerosis as well as cardiovascular event rates (for review, see Munzel et al1) Although the mechanisms underlying this phenomenon are complex and multifactorial, there is growing body of evidence that oxidative stress attributable to increased production of reactive oxygen–derived free radicals may play a pivotal role in this process.2 Increased superoxide production by enzyme systems such as the…

Vitaminmedicine.medical_specialtybusiness.industryVitamin Emedicine.medical_treatmentmedicine.diseasemedicine.disease_causeCalcitriol receptorchemistry.chemical_compoundB vitaminsEndocrinologychemistryInternal medicineDiabetes mellitusInternal MedicinemedicineEndothelial dysfunctionbusinessNicotinamide adenine dinucleotide phosphateOxidative stressHypertension
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Modulatory Role of Endothelial and Nonendothelial Nitric Oxide in 5-Hydroxytryptamine-induced Contraction in Cerebral Arteries after Subarachnoid Hem…

1996

OBJECTIVE : Endothelial dysfunction is claimed to play a role in the pathogenesis of delayed cerebral vasospasm after subarachnoid hemorrhage (SAH). We have examined the effect of experimental SAH on the modulatory action of endothelial and nonendothelial nitric oxide (NO) in the contractile response of goat middle cerebral artery to 5-hydroxytryptamine (5-HT). METHODS : We compared the 5-HT-induced contractile responses of cerebral arteries from control goats and from goats with SAH that had been experimentally induced 3 days earlier by delivery of autologous arterial blood into the subarachnoid space. Contractile responses were examined by recording the isometric tension in isolated cereb…

Serotoninmedicine.medical_specialtySubarachnoid hemorrhageEndotheliumCerebral arteriesNitric OxideCerebral vasospasmReference Valuesmedicine.arteryInternal medicinemedicineAnimalscardiovascular diseasesEndothelial dysfunctionVascular diseasebusiness.industryGoatsCerebral ArteriesSubarachnoid Hemorrhagemedicine.diseasenervous system diseasesmedicine.anatomical_structureEndocrinologyVasoconstrictionAnesthesiaMiddle cerebral arteryFemaleSurgeryEndothelium VascularNeurology (clinical)businessBlood vesselNeurosurgery
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The sodium-glucose co-transporter 2 inhibitor empagliflozin improves diabetes-induced vascular dysfunction in the streptozotocin diabetes rat model b…

2014

Objective In diabetes, vascular dysfunction is characterized by impaired endothelial function due to increased oxidative stress. Empagliflozin, as a selective sodium-glucose co-transporter 2 inhibitor (SGLT2i), offers a novel approach for the treatment of type 2 diabetes by enhancing urinary glucose excretion. The aim of the present study was to test whether treatment with empagliflozin improves endothelial dysfunction in type I diabetic rats via reduction of glucotoxicity and associated vascular oxidative stress. Methods Type I diabetes in Wistar rats was induced by an intravenous injection of streptozotocin (60 mg/kg). One week after injection empagliflozin (10 and 30 mg/kg/d) was adminis…

Blood GlucoseMalemedicine.medical_treatmentReceptor for Advanced Glycation End Productslcsh:MedicineGene ExpressionType 2 diabetesmedicine.disease_causeVascular MedicineGlucosidesMedicine and Health SciencesMedicineInsulinEndothelial dysfunctionReceptors Immunologiclcsh:ScienceMultidisciplinaryType 1 DiabetesCytokinesInflammation Mediatorsmedicine.drugSignal TransductionResearch Articlemedicine.medical_specialtyCardiologyBlood sugarStreptozocinCardiovascular PharmacologyDiabetes Mellitus ExperimentalDiabetes ComplicationsInternal medicineDiabetes mellitusEmpagliflozinDiabetes MellitusAnimalsRNA MessengerVascular DiseasesBenzhydryl CompoundsSodium-Glucose Transporter 2 InhibitorsPharmacologybusiness.industryInsulinlcsh:RHemodynamicsStreptozotocinmedicine.diseaseRatsOxidative StressEndocrinologyGlucoseMetabolic Disorderslcsh:QbusinessOxidative stressDiabetic AngiopathiesPloS one
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Targeting antioxidants to mitochondria: a potential new therapeutic strategy for cardiovascular diseases.

2007

Mitochondria produce large amounts of free radicals and play an important role in the life and death of a cell. Thus, mitochondrial oxidative damage and dysfunction contribute to a number of cell pathologies that manifest themselves through a range of conditions including ischemia-reperfusion injury, sepsis, diabetes, atherosclerosis and, consequently, cardiovascular diseases (CVD). In fact, endothelial dysfunction, characterized by a loss of nitric oxide (NO) bioactivity, occurs early on in the development of atherosclerosis, and determines future vascular complications. Although the molecular mechanisms responsible for mitochondria-mediated disease processes are not yet clear, oxidative s…

Oxidative phosphorylationPharmacologyMitochondrionBiologymedicine.disease_causeAntioxidantsNitric oxidechemistry.chemical_compoundDrug DiscoverymedicineAnimalsHumansEndothelial dysfunctionInner mitochondrial membranePharmacologychemistry.chemical_classificationReactive oxygen speciesMolecular Structuremedicine.diseaseMitochondriaOxidative StresschemistryCardiovascular DiseasesReactive Oxygen SpeciesReperfusion injuryOxidative stressCurrent pharmaceutical design
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New Therapeutic Implications of Endothelial Nitric Oxide Synthase (eNOS) Function/Dysfunction in Cardiovascular Disease

2019

The Global Burden of Disease Study identified cardiovascular risk factors as leading causes of global deaths and life years lost. Endothelial dysfunction represents a pathomechanism that is associated with most of these risk factors and stressors, and represents an early (subclinical) marker/predictor of atherosclerosis. Oxidative stress is a trigger of endothelial dysfunction and it is a hall-mark of cardiovascular diseases and of the risk factors/stressors that are responsible for their initiation. Endothelial function is largely based on endothelial nitric oxide synthase (eNOS) function and activity. Likewise, oxidative stress can lead to the loss of eNOS activity or even “uncoupli…

0301 basic medicineAdipose tissueReview030204 cardiovascular system & hematologyPharmacologymedicine.disease_causeendothelial dysfunctionEpigenesis Geneticlcsh:Chemistry0302 clinical medicineEnoscardiovascular diseaseeNOS uncouplingoxidative stressEndothelial dysfunctionlcsh:QH301-705.5Spectroscopyenvironmental stressorsbiologyGeneral MedicineComputer Science Applicationsmedicine.anatomical_structureCardiovascular Diseasesmedicine.symptomOxidation-ReductionCell signalingEndotheliumNitric Oxide Synthase Type IIIInflammationModels BiologicalCatalysisInorganic Chemistry03 medical and health scienceslife style/behavioral health risk factorsmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular Biologybusiness.industryOrganic Chemistrymedicine.diseasebiology.organism_classification030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Socioeconomic FactorsinflammationSoluble guanylyl cyclasebusinessOxidative stressInternational Journal of Molecular Sciences
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THE METABOLIC SYNDROME IN HYPERTENSION

2019

The metabolic syndrome (MS) is currently considered to be a cluster of metabolic and cardiovascular risk factors including blood pressure elevation. A higher risk to develop hypertension in MS subjects with high-normal blood pressure has been observed and, when hypertension is established, seems to be what confers a higher cardiovascular risk on top of the risk induced by blood pressure elevation. Therefore, assessment of MS components can result in clinical utility strategy to manage hypertension based on individual risk. The main mechanisms for blood pressure elevation include overactivity of the sympathetic and the reninangiotensin system, abnormal renal sodium handling, and endothelial …

medicine.medical_specialtymedicine.diagnostic_testbusiness.industrymedicine.diseaseInsulin resistanceBlood pressureEndocrinologyInternal medicineDiabetes mellitusPathophysiology of hypertensionAortic pressureCardiologyMedicineEndothelial dysfunctionMetabolic syndromebusinessLipid profile
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