Search results for "NITRIC OXIDE SYNTHASE"

showing 10 items of 531 documents

Role of NO-synthases and cyclooxygenases in the hyperreactivity of male rabbit carotid artery to testosterone under experimental diabetes.

2009

Abstract Cardiovascular disease is the major cause of morbidity and mortality in diabetic patients, which in turn is also associated with low levels of serum testosterone. The working hypothesis was that diabetes might modify the mechanisms involved in the vascular actions of testosterone in isolated rabbit carotid arteries. Testosterone (10 −8 –3 × 10 −4  M) induced a concentration-dependent relaxation of precontracted carotid arteries, which was higher in diabetic than in control rabbits. In control rabbits neither endothelium removal nor the nitric oxide synthase (NOS) inhibitor N G -nitro- l -arginine ( l -NOArg, 10 −5  M) modified the relaxant action of testosterone, and the cyclooxyge…

Blood GlucoseCarotid Artery DiseasesMalemedicine.medical_specialtyArginineEndotheliumCharybdotoxinNitric Oxide Synthase Type IIIThromboxaneBlotting WesternIndomethacinNitric Oxide Synthase Type IIVasodilationProstacyclinNitric OxideNitroarginineDiabetes Mellitus ExperimentalImmunoenzyme TechniquesThromboxane A2Internal medicinemedicinePotassium Channel BlockersAnimalsCyclooxygenase InhibitorsTestosteronePharmacologybiologyDose-Response Relationship Drugbusiness.industryTestosterone (patch)EpoprostenolNitric oxide synthaseVasodilationEndocrinologymedicine.anatomical_structureCarotid ArteriesApaminCyclooxygenase 2cardiovascular systembiology.proteinPotassiumCalciumCyclooxygenaseEndothelium VascularRabbitsbusinessDiabetic Angiopathiesmedicine.drugPharmacological research
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High pancreatic n-3 fatty acids prevent STZ-induced diabetes in fat-1 mice: inflammatory pathway inhibition.

2011

OBJECTIVE Because of confounding factors, the effects of dietary n-3 polyunsaturated fatty acids (PUFA) on type 1 diabetes remain to be clarified. We therefore evaluated whether fat-1 transgenic mice, a well-controlled experimental model endogenously synthesizing n-3 PUFA, were protected against streptozotocin (STZ)-induced diabetes. We then aimed to elucidate the in vivo response at the pancreatic level. RESEARCH DESIGN AND METHODS β-Cell destruction was produced by multiple low-doses STZ (MLD-STZ). Blood glucose level, plasma insulin level, and plasma lipid analysis were then performed. Pancreatic mRNA expression of cytokines, the monocyte chemoattractant protein, and GLUT2 were evaluate…

Blood GlucoseFatty Acid DesaturasesMalemedicine.medical_specialtyEndocrinology Diabetes and Metabolismmedicine.medical_treatmentBlotting WesternMice TransgenicBiologyProinflammatory cytokineDiabetes Mellitus Experimentalchemistry.chemical_compoundMiceInternal medicineFatty Acids Omega-3Internal MedicinemedicineAnimalsInsulinCaenorhabditis elegans ProteinsUnsaturated fatty acidLipoxinReverse Transcriptase Polymerase Chain ReactionInsulinTranscription Factor RelAStreptozotocinImmunohistochemistryLipidsNitric oxide synthasemedicine.anatomical_structureEndocrinologyMetabolismchemistryHyperglycemiabiology.proteinGLUT2FemalePancreasmedicine.drugSignal TransductionDiabetes
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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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Time course of asymmetric dimethylarginine (ADMA) and oxidative stress in fructose-hypertensive rats: A model related to metabolic syndrome

2011

Asymmetric dimethylarginine (ADMA) is an endogenous modulator of endothelial function and oxidative stress, and increased levels of this molecule have been reported in some metabolic disorders and cardiovascular diseases. The aim of this work was to analyze the time course of dimethylarginine compounds and oxidative stress levels and the relationship between these and cardiovascular function in fructose-hypertensive rats.90 male Sprague-Dawley rats were randomized into 2 groups, fed for 3 months with standard (C) chow supplemented or not with fructose (F, 60%). After sacrifice at different weeks (W), the aorta and plasma were harvested to assess the vascular and biochemical parameters. Our …

Blood GlucoseMaleTime FactorsVasodilator AgentsNitric Oxide Synthase Type IIBlood Pressure030204 cardiovascular system & hematologymedicine.disease_causeRats Sprague-Dawleychemistry.chemical_compound0302 clinical medicineHeart RateEnzyme InhibitorsAortaComputingMilieux_MISCELLANEOUSMetabolic Syndrome0303 health sciencesOxidase testVasodilationNAD(P)H oxidaseHypertensionCardiology and Cardiovascular Medicinemedicine.medical_specialtyFructoseArginine03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicinemedicine.arterymedicineAnimals030304 developmental biologyAortaDose-Response Relationship Drugbusiness.industryVascular diseaseBody WeightNADPH OxidasesFructosemedicine.diseaseRatsDisease Models AnimalOxidative StressEndocrinologychemistryTyrosineMetabolic syndromebusinessAsymmetric dimethylarginineOxidative stressAtherosclerosis
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Mechanisms involved in the relaxant action of testosterone in the renal artery from male normoglycemic and diabetic rabbits.

2009

Kidney disease is a frequent complication in diabetes, and significant differences have been reported between male and female patients. Our working hypothesis was that diabetes might modify the vascular actions of testosterone in isolated rabbit renal arteries and the mechanisms involved in these actions. Testosterone (10(-8) to 10(-4)M) induced relaxation of precontracted arteries, without significant differences between control and diabetic rabbits. Both in control and diabetic rabbits endothelium removal inhibited testosterone relaxant action. In arteries with endothelium, incubation with indomethacin (10(-5)M), N(G)-nitro-l-arginine (10(-5)M) or tetraethylammonium (10(-5)M) did not modi…

Blood GlucoseMalemedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIIThromboxaneBlotting WesternIndomethacinNitric Oxide Synthase Type IIProstacyclinVasodilationNitroarginineMuscle Smooth VascularDiabetes Mellitus ExperimentalImmunoenzyme TechniquesThromboxane A2Renal ArteryEnosInternal medicinemedicine.arteryDiabetes mellitusmedicinePotassium Channel BlockersAnimalsCyclooxygenase InhibitorsProstaglandins ITestosteroneRenal arteryPharmacologybiologyDose-Response Relationship Drugbusiness.industryTetraethylammoniumTestosterone (patch)medicine.diseasebiology.organism_classificationVasodilationEndocrinologymedicine.anatomical_structureCyclooxygenase 2Cyclooxygenase 1PotassiumCalciumEndothelium VascularRabbitsbusinessmedicine.drugSignal TransductionPharmacological research
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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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Heme oxygenase-1 induction and regulation in unstimulated mouse peritoneal macrophages

2003

Heme oxygenase-1 (HO-1) is a stress protein induced by a variety of stimuli in inflammatory cells. This study was set up to investigate the induction of this protein in unstimulated macrophages. Resident mouse peritoneal macrophages purified by adhesion and cultured in basal conditions strongly induced HO-1 in a time-dependent manner, with a peak at 20 hr. At the same time, low levels of nitrite accumulated in the culture medium and expression of nitric oxide synthase-2 (NOS-2) and NOS-3 protein was detected. Inhibition of NO production and/or NOS expression by incubating macrophages with different drugs inhibiting NOS activity or modulating the redox state of the cell, such as N-acetylcyst…

Blotting WesternInflammationNitric Oxidemedicine.disease_causeBiochemistryNitric oxideMicechemistry.chemical_compoundmedicineAnimalsMacrophageHemeCells CulturedPharmacologybiologyChemistryMembrane ProteinsEndogenous mediatorImmunohistochemistryCell biologyNitric oxide synthaseHeme oxygenaseBiochemistryEnzyme InductionHeme Oxygenase (Decyclizing)Macrophages Peritonealbiology.proteinNitric Oxide Synthasemedicine.symptomOxidation-ReductionHeme Oxygenase-1Oxidative stressBiochemical Pharmacology
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Cyclic AMP-mediated upregulation of the expression of neuronal NO synthase in human A673 neuroepithelioma cells results in a decrease in the level of…

2004

The expression level of neuronal nitric oxide synthase (nNOS) can vary depending on the (patho)physiological conditions. Here we document a marked induction of nNOS mRNA, protein, and total NO production in response to dibutyryl cyclic AMP (db-cAMP) in human A673 neuroepithelial cells. However, the upregulation of nNOS was associated with a decreased level of production of bioactive NO and by an increase in the level of generation of reactive oxygen species (ROS). ROS production could be prevented by the NOS inhibitor L-NAME, suggesting nNOS itself is involved in ROS generation. Sepiapterin supplementation of db-cAMP-treated A673 cells could restore full bioactive NO production, most likely…

CAMP-Responsive Element ModulatorNitric Oxide Synthase Type IBiologyCREBNitric OxideBiochemistryAdenylyl cyclaseCyclic AMP Response Element Modulatorchemistry.chemical_compoundMiceNeuroblastomaCoactivatorComplement C3b Inactivator ProteinsCyclic AMPAnimalsHumansNeuroectodermal Tumors Primitive PeripheralCREB-binding proteinEnzyme InhibitorsProtein kinase AeducationCyclic AMP Response Element-Binding ProteinGTP CyclohydrolaseCAMP response element bindingHomeodomain ProteinsNeuronseducation.field_of_studyForskolinPhosphoric Diester HydrolasesIntracellular Signaling Peptides and ProteinsBlood ProteinsLIM Domain ProteinsMolecular biologyCyclic AMP-Dependent Protein KinasesPterinsUp-RegulationDNA-Binding ProteinsRepressor ProteinsAntisense Elements (Genetics)NG-Nitroarginine Methyl EsterchemistryBucladesineGene Expression RegulationComplement Factor Hbiology.proteinNitric Oxide SynthaseReactive Oxygen SpeciesSignal TransductionBiochemistry
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Analysis of parathyroid graft rejection suggests alloantigen-specific production of nitric oxide by iNOS-positive intragraft macrophages

2009

Abstract Background During acute rejection of organ or tissue allografts T cells and macrophages are dominant infiltrating cells. CD4-positive T cells are important for the induction of allograft rejection and macrophages are important effector cells mediating cytotoxicity via production of nitric oxide (NO) by the inducible NO-synthase (iNOS). In the present study we analysed whether the destruction of primarily nonvascularised parathyroid allografts is also mediated by iNOS-positive macrophages. Methods Hypocalcaemic Lewis rats received parathyroid isografts (from Lewis donors) and allografts (from Wistar Furth donors), respectively, under the kidney capsule. Levels of serum calcium above…

CD4-Positive T-LymphocytesGraft RejectionMaleImmunologyThyroid GlandNitric Oxide Synthase Type IIRats Inbred WFInflammationCell CommunicationLymphocyte ActivationMajor histocompatibility complexNitric oxidechemistry.chemical_compoundAntigenCell MovementHistocompatibility AntigensmedicineAnimalsTransplantation HomologousImmunology and AllergyCytotoxic T cellMacrophageTransplantationbiologyChemistryMacrophage ActivationAntigens DifferentiationPeptide FragmentsRatsEnzyme ActivationTransplantationMononuclear cell infiltrationGene Expression RegulationRats Inbred LewImmunologyDisease ProgressionMacrophages Peritonealbiology.proteinCalciumImmunizationmedicine.symptomTransplant Immunology
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