Search results for " Type II"

showing 10 items of 542 documents

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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eNOS Uncoupling in Cardiovascular Diseases - the Role of Oxidative Stress and Inflammation

2013

Many cardiovascular diseases and drug-induced complications are associated with - or even based on - an imbalance between the formation of reactive oxygen and nitrogen species (RONS) and antioxidant enzymes catalyzing the break-down of these harmful oxidants. According to the “kindling radical” hypothesis, the formation of RONS may trigger in certain conditions the activation of additional sources of RONS. According to recent reports, vascular dysfunction in general and cardiovascular complications such as hypertension, atherosclerosis and coronary artery diseases may be connected to inflammatory processes. The present review is focusing on the uncoupling of endothelial nitric oxide synthas…

medicine.medical_specialtyNitric Oxide Synthase Type IIIInflammationOxidative phosphorylationmedicine.disease_causechemistry.chemical_compoundEnosInternal medicineDrug DiscoverymedicineHumansEndothelial dysfunctionInflammationPharmacologybiologyTetrahydrobiopterinbiology.organism_classificationmedicine.diseaseReview articleOxidative StressEndocrinologychemistryCardiovascular Diseasesmedicine.symptomAsymmetric dimethylarginineOxidative stressmedicine.drugCurrent Pharmaceutical Design
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Dexamethasone suppresses eNOS and CAT-1 and induces oxidative stress in mouse resistance arterioles

2004

Long-term treatment with glucocorticoids is associated with mild to moderate hypertension. We reported previously that downregulation of endothelial NO synthase (eNOS) expression and activity is likely to contribute to this increase in blood pressure. In the present study, we tested the effects of dexamethasone on the vasodilation of microvascular arterioles using implanted dorsal skin-fold chambers in anesthetized C57BL/6J mice. Experiments were performed on control mice or on mice treated with dexamethasone (0.1–3 mg/kg of body wt). Endothelium-dependent vasodilation in response to ACh (0.1–10 μM) was reduced by dexamethasone in a dose-dependent fashion. Comparable inhibition was seen in …

medicine.medical_specialtyNitric Oxide Synthase Type IIIPhysiologyNitric Oxide Synthase Type IIAscorbic AcidBiologyArgininemedicine.disease_causeAntioxidantsDexamethasoneMicrocirculationMiceDownregulation and upregulationEnosArteriolePhysiology (medical)medicine.arteryInternal medicinemedicineAnimalsHumansGlucocorticoidsCells CulturedNitritesDexamethasoneCationic Amino Acid Transporter 1NitratesMyocardiumEndothelial Cellsbiology.organism_classificationAcetylcholineMice Inbred C57BLVasodilationNitric oxide synthaseArteriolesOxidative StressEndocrinologybiology.proteinVascular ResistanceNitric Oxide SynthaseCardiology and Cardiovascular MedicineOxidative stressGlucocorticoidmedicine.drugAmerican Journal of Physiology-Heart and Circulatory Physiology
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PPARγ as an indicator of vascular function in an experimental model of metabolic syndrome in rabbits

2021

Abstract Background and aims Underlying mechanisms associated with vascular dysfunction in metabolic syndrome (MetS) remain unclear and can even vary from one vascular bed to another. Methods In this study, MetS was induced by a high-fat, high-sucrose diet, and after 28 weeks, aorta and renal arteries were removed and used for isometric recording of tension in organ baths, protein expression by Western blot, and histological analysis to assess the presence of atherosclerosis. Results MetS induced a mild hypertension, pre-diabetes, central obesity and dyslipidaemia. Our results indicated that MetS did not change the contractile response in either the aorta or renal artery. Conversely, vasodi…

medicine.medical_specialtyNitric Oxide Synthase Type IIIVasodilationmedicine.disease_causeEnosmedicine.arteryInternal medicineAnimalsMedicineRenal arteryProtein kinase BSistema cardiovascularMetabolic SyndromeAortaDiabetisbiologybusiness.industryModels Theoreticalmedicine.diseasebiology.organism_classificationPPAR gammaVasodilationEndocrinologyEndothelium VascularRabbitsSodium nitroprussideMetabolic syndromeCardiology and Cardiovascular MedicinebusinessProto-Oncogene Proteins c-aktOxidative stressmedicine.drugAtherosclerosis
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Orthopedic manifestations in patients with mucopolysaccharidosis type II (Hunter syndrome) enrolled in the Hunter Outcome Survey.

2010

Mucopolysaccharidosis type II (MPS II or Hunter syndrome) is a rare, inherited disorder caused by deficiency of the lysosomal enzyme iduronate-2-sulfatase. As a result of this deficiency, glycosaminoglycans accumulate in lysosomes in many tissues, leading to progressive multisystemic disease. The cardiopulmonary and neurological problems associated with MPS II have received considerable attention. Orthopedic manifestations are common but not as well characterized. This study aimed to characterize the prevalence and severity of orthopedic manifestations of MPS II and to determine the relationship of these signs and symptoms with cardiovascular, pulmonary and central nervous system involvemen…

medicine.medical_specialtyPediatricsspine.MucopolysaccharidosisDiseaseboneArticlebone joint mucopolysaccharidosis orthopedic spinejointmedicineOrthopedics and Sports MedicineMucopolysaccharidosis type IIorthopedicOrthopedic surgerybusiness.industryHunter syndromemucopolysaccharidosismedicine.diseaseSurgeryNatural historymedicine.anatomical_structureOrthopedic surgeryAnkleRange of motionbusinessRD701-811Orthopedic reviews
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Exercise restores decreased physical activity levels and increases markers of autophagy and oxidative capacity in myostatin/activin blocked mdx mice

2013

The importance of adequate levels of muscle size and function and physical activity is widely recognized. Myostatin/activin blocking increases skeletal muscle mass but may decrease muscle oxidative capacity and can thus be hypothesized to affect voluntary physical activity. Soluble activin receptor IIB (sActRIIB-Fc) was produced to block myostatin/activins. Modestly dystrophic mdx mice were injected with sActRIIB-Fc or PBS with or without voluntary wheel running exercise for 7 wk. Healthy mice served as controls. Running for 7 wk attenuated the sActRIIB-Fc-induced increase in body mass by decreasing fat mass. Running also enhanced/restored the markers of muscle oxidative capacity and autoph…

medicine.medical_specialtyPhysiologyActivin Receptors Type IIEndocrinology Diabetes and MetabolismBlotting WesternCitrate (si)-SynthaseMyostatinMotor ActivityHematocritMuscle hypertrophyEatingHemoglobinsMice03 medical and health sciences0302 clinical medicinePhysical Conditioning AnimalPhysiology (medical)Internal medicineAutophagymedicineAnimalsMuscle Skeletalta315Creatine KinaseAdiposity030304 developmental biology0303 health sciencesbiologymedicine.diagnostic_testTumor Necrosis Factor-alphaBody WeightAutophagySkeletal muscleDNAActivin receptorMyostatinActivinsMice Inbred C57BLmedicine.anatomical_structureEndocrinologyHematocritMice Inbred mdxbiology.proteinCreatine kinaseTumor necrosis factor alphaOxidation-Reduction030217 neurology & neurosurgeryAmerican Journal of Physiology-Endocrinology and Metabolism
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Translational Research for Improving the Care of Familial Hypercholesterolemia: The “Ten Countries Study” and Beyond

2016

Familial hypercholesterolemia (FH) is the most common and serious form of inherited hyperlipidaemia. Dominantly inherited with high penetrance, untreated FH leads to premature death from coronary artery disease due to accelerated atherosclerosis from birth. Despite its importance, there is still a major shortfall in awareness, detection and treatment of FH worldwide. International models of care for FH have recently been published, but their effective implementation requires the garnering of more knowledge about the condition. The "Ten Countries Study" aims to investigate diagnostic, epidemiological and service aspects, as well as physician practices and patient experiences of FH in several…

medicine.medical_specialtyPrevalenceAlternative medicineTranslational researchReviewFamilial hypercholesterolemia030204 cardiovascular system & hematologyHyperlipoproteinemia Type IITranslational Research BiomedicalCoronary artery disease03 medical and health sciences0302 clinical medicineEpidemiologyInternal MedicinemedicineHumans030212 general & internal medicineQuality of Health Carebusiness.industryBiochemistry (medical)medicine.diseaseFamily medicinePhysical therapyObservational studyPersonal experienceCardiology and Cardiovascular MedicinebusinessJournal of Atherosclerosis and Thrombosis
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Nitric oxide triggers mammary gland involution after weaning: remodelling is delayed but not impaired in mice lacking inducible nitric oxide synthase

2010

During mammary gland involution, different signals are required for apoptosis and tissue remodelling. To explore the role of NO in the involution of mammary tissue after lactation, NOS2 (inducible nitric oxide synthase)-KO (knockout) mice were used. No apparent differences were observed between NOS2-KO and WT (wild-type) animals during pregnancy and lactation. However, upon cessation of lactation, a notable delay in involution was observed, compared with WT mice. NOS2-KO mice showed increased phosphorylation of STAT (signal transducer and activator of transcription) 5 during weaning, concomitant with increased beta-casein mRNA levels when compared with weaned WT glands, both hallmarks of th…

medicine.medical_specialtyProgrammed cell deathNitric Oxide Synthase Type IIWeaningBiologyNitric OxideBiochemistryNitric oxideMicechemistry.chemical_compoundMammary Glands AnimalInternal medicinemedicineAnimalsInvolution (medicine)STAT3Molecular BiologyMammary gland involutionMice KnockoutCell BiologyAnimals SucklingProlactinMice Inbred C57BLNitric oxide synthaseEndocrinologychemistryApoptosisbiology.proteinSTAT proteinFemaleBiochemical Journal
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Estradiol, acting through estrogen receptor alpha, restores dimethylarginine dimethylaminohydrolase activity and nitric oxide production in oxLDL-tre…

2011

Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) synthase. ADMA accumulation, mainly due to a decreased dimethylarginine dimethylaminohydrolase (DDAH) activity, has been related to the development of cardiovascular diseases. We investigate whether estradiol prevents the changes induced by oxidized low density lipoprotein (oxLDL) on the DDAH/ADMA/NO pathway in human umbilical artery endothelial cells (HUAEC). HUAEC were exposed to estradiol, native LDL (nLDL), oxLDL and their combinations for 24 h. In some experiments, cells were also exposed to the unspecific estrogen receptor (ER) antagonist ICI 182780, the specific ERα antagonist MPP or specific agonists …

medicine.medical_specialtyProtein-Arginine N-MethyltransferasesEndotheliumNitric Oxide Synthase Type IIImedicine.drug_classBlotting WesternArginineNitric OxideBiochemistryUmbilical ArteriesNitric oxideAmidohydrolasesReceptors G-Protein-Coupledchemistry.chemical_compoundEndocrinologyEnosInternal medicinemedicineEstrogen Receptor betaHumansEstrogens Non-SteroidalMolecular BiologyCells CulturedbiologyEstradiolArtèriesProtein StabilityEstrogen AntagonistsEstrogen Receptor alphaEndoteli vascularbiology.organism_classificationNitric oxide synthaseIsoenzymesLipoproteins LDLRepressor Proteinsmedicine.anatomical_structureEndocrinologychemistryReceptors EstrogenEstrogenbiology.proteinlipids (amino acids peptides and proteins)Endothelium VascularAsymmetric dimethylarginineEstrogen receptor alphaGPER
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Biopterin metabolism and eNOS expression during hypoxic pulmonary hypertension in mice.

2013

International audience; Tetrahydrobiopterin (BH$_4$), which fosters the formation of and stabilizes endothelial NO synthase (eNOS) as an active dimer, tightly regulates eNOS coupling / uncoupling. Moreover, studies conducted in genetically-modified models demonstrate that BH$_4$ pulmonary deficiency is a key determinant in the pathogenesis of pulmonary hypertension. The present study thus investigates biopterin metabolism and eNOS expression, as well as the effect of sepiapterin (a precursor of BH$_4$) and eNOS gene deletion, in a mice model of hypoxic pulmonary hypertension. In lungs, chronic hypoxia increased BH$_4$ levels and eNOS expression, without modifying dihydrobiopterin (BH$_2$, t…

medicine.medical_specialtySepiapterinNitric Oxide Synthase Type III[SDV]Life Sciences [q-bio]Hypertension PulmonaryBiopterinlcsh:Medicine[SDV.BC]Life Sciences [q-bio]/Cellular Biology[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]030204 cardiovascular system & hematology03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineEnosRight ventricular hypertrophyDihydrobiopterinInternal medicinemedicine[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]AnimalsHypoxialcsh:Science[SDV.BC] Life Sciences [q-bio]/Cellular Biology030304 developmental biology0303 health sciencesMultidisciplinarybiologylcsh:RHypoxia (medical)biology.organism_classificationmedicine.diseasePulmonary hypertensionBiopterin[SDV] Life Sciences [q-bio]Disease Models AnimalTetrahydrofolate DehydrogenaseEndocrinologychemistryVentricular pressurelcsh:Qmedicine.symptomResearch ArticlePLoS ONE
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