Search results for "type II"

showing 10 items of 607 documents

Association between phenotypic familial hypercholesterolaemia and telomere length in US adults: results from a multi-ethnic survey

2018

Aims: Familial hypercholesterolaemia (FH) accelerates atherosclerotic cardiovascular disease (ASCVD) and accordingly is the most potent hereditary cause of premature coronary heart disease. The association between telomere length (TL), a biological index of ageing, and FH has not been hitherto investigated. We addressed this question using data from the US National Health and Education National Surveys (NHANES, 1999-2002).Methods and results: We included individuals, who had TL measurements (with quantitative polymerase chain reaction method) and a phenotypic diagnosis of FH based on the Dutch Lipid Clinic Network (DLCN) criteria. Sample weights were applied for unequal probabilities of sel…

Malemedicine.medical_specialtyNational Health and Nutrition Examination SurveyCross-sectional studyPopulationFamilial hypercholesterolemia030204 cardiovascular system & hematologyHyperlipoproteinemia Type II03 medical and health sciences0302 clinical medicineInternal medicineMedicineHumans030212 general & internal medicineeducationNational Health and Education National Surveyseducation.field_of_studyTelomere lengthbusiness.industryMiddle AgedTelomeremedicine.diseaseNutrition SurveysObesityConfidence intervalUnited StatesCross-Sectional StudiesQuartileFemaleCardiology and Cardiovascular MedicinebusinessFamilial hypercholesterolaemiaBody mass indexEuropean Heart Journal
researchProduct

Down-regulation of the expression of endothelial NO synthase is likely to contribute to glucocorticoid-mediated hypertension.

1999

Hypertension is a side effect of systemically administered glucocorticoids, but the underlying molecular mechanism remains poorly understood. Ingestion of dexamethasone by rats telemetrically instrumented increased blood pressure progressively over 7 days. Plasma concentrations of Na + and K + and urinary Na + and K + excretion remained constant, excluding a mineralocorticoid-mediated mechanism. Plasma NO 2 − /NO 3 − (the oxidation products of NO) decreased to 40%, and the expression of endothelial NO synthase (NOS III) was found down-regulated in the aorta and several other tissues of glucocorticoid-treated rats. The vasodilator response of resistance arterioles was tested by intravital m…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIDown-RegulationVasodilationBiologyEndothelial NOSRats Inbred WKYUmbilical veinDexamethasonechemistry.chemical_compoundInternal medicinemedicineAnimalsRNA MessengerPromoter Regions GeneticAortaCells CulturedNitritesDNA PrimersMultidisciplinaryNitratesBase SequenceAntiglucocorticoidNitric Oxide Synthase Type IIIBiological SciencesRatsNitric oxide synthaseVasodilationEndocrinologychemistryHypertensionbiology.proteinEndothelium VascularNitric Oxide SynthaseGlucocorticoidIntravital microscopymedicine.drugTranscription FactorsProceedings of the National Academy of Sciences of the United States of America
researchProduct

Cannabinoid type 1 receptor blockade promotes mitochondrial biogenesis through endothelial nitric oxide synthase expression in white adipocytes

2008

OBJECTIVE—Cannabinoid type 1 (CB1) receptor blockade decreases body weight and adiposity in obese subjects; however, the underlying mechanism is not yet fully understood. Nitric oxide (NO) produced by endothelial NO synthase (eNOS) induces mitochondrial biogenesis and function in adipocytes. This study was undertaken to test whether CB1 receptor blockade increases the espression of eNOS and mitochondrial biogenesis in white adipocytes. RESEARCH DESIGN AND METHODS—We examined the effects on eNOS and mitochondrial biogenesis of selective pharmacological blockade of CB1 receptors by SR141716 (rimonabant) in mouse primary white adipocytes. We also examined eNOS expression and mitochondrial biog…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndocrinology Diabetes and MetabolismAdipocytes WhiteImmunoblottingCitrate (si)-SynthaseWhite adipose tissueAMP-Activated Protein KinasesProtein Serine-Threonine KinasesMitochondrionDNA MitochondrialMicechemistry.chemical_compoundAdenosine TriphosphatePiperidinesReceptor Cannabinoid CB1AMP-activated protein kinaseMultienzyme ComplexesEnosAdipocyteInternal medicineInternal MedicinemedicineAnimalsPhosphorylationRNA Small InterferingReceptorCells CulturedDose-Response Relationship DrugbiologyReverse Transcriptase Polymerase Chain ReactionFlow Cytometrybiology.organism_classificationMitochondriaMice Inbred C57BLNitric oxide synthaseMetabolismEndocrinologychemistryMitochondrial biogenesisbiology.proteinSettore BIO/14 - FarmacologiaPyrazolesRimonabant
researchProduct

Regulation of Oxygen Distribution in Tissues by Endothelial Nitric Oxide

2009

Nitric oxide (NO) decreases cellular oxygen (O 2 ) consumption by competitively inhibiting cytochrome c oxidase. Here, we show that endogenously released endothelial NO, either basal or stimulated, can modulate O 2 consumption both throughout the thickness of conductance vessels and in the microcirculation. Furthermore, we have shown that such modulation regulates O 2 distribution to the surrounding tissues. We have demonstrated these effects by measuring O 2 consumption in blood vessels in a hypoxic chamber and O 2 distribution in the microcirculation using the fluorescent oxygen-probe Ru(phen) 3 2+ . Removal of NO by physical or pharmacological means, or in eNOS −/− mice, abolishes this …

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumPhysiologychemistry.chemical_elementOxygen consumptionBiologyNitric OxideOxygenMicrocirculationNitric oxideElectron Transport Complex IVRats Sprague-DawleyMicechemistry.chemical_compoundOxygen Consumption:CIENCIAS MÉDICAS ::Medicina interna [UNESCO]EnosInternal medicinemedicineAnimalsHumansCytochrome c oxidaseEndotheliumHypoxiaUNESCO::CIENCIAS MÉDICAS ::Medicina internaMice KnockoutNitric Oxide Synthase Type IIINitric oxide:CIENCIAS MÉDICAS [UNESCO]biology.organism_classificationRatsOxygenEndocrinologymedicine.anatomical_structurechemistryUNESCO::CIENCIAS MÉDICASCirculatory systemBiophysicsbiology.proteinNitric oxide ; Endothelium ; Oxygen consumptionEndothelium VascularCardiology and Cardiovascular MedicineSignal TransductionCirculation Research
researchProduct

Mechanisms underlying recoupling of eNOS by HMG-CoA reductase inhibition in a rat model of streptozotocin-induced diabetes mellitus

2007

Abstract Objective HMG-CoA reductase inhibitors have been shown to upregulate GTP cyclohydrolase I (GTPCH-I), the key enzyme for tetrahydrobiopterin de novo synthesis and to normalize tetrahydrobiopterin levels in hyperglycemic endothelial cells. We sought to determine whether in vivo treatment with the HMG-CoA reductase inhibitor atorvastatin is able to upregulate the GTPCH-I, to recouple eNOS and to normalize endothelial dysfunction in an experimental model of diabetes mellitus. Methods and results In male Wistar rats, diabetes was induced by streptozotocin (STZ, 60mg/kg). In STZ rats, atorvastatin feeding (20mg/kg/d, 7 weeks), normalized vascular dysfunction as analyzed by isometric tens…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIGTP cyclohydrolase INitric Oxide Synthase Type IIReductaseArticleDiabetes Mellitus ExperimentalCytochrome P-450 Enzyme SystemEnosInternal medicineAtorvastatinmedicineAnimalsNADH NADPH OxidoreductasesPyrrolesRats WistarEndothelial dysfunctionGTP CyclohydrolaseNADPH oxidasebiologyStem CellsBody WeightMicrofilament ProteinsTetrahydrobiopterinPhosphoproteinsmedicine.diseasebiology.organism_classificationBiopterinRatsEnzyme ActivationIntramolecular OxidoreductasesVasodilationNitric oxide synthaseDisease Models AnimalOxidative StressTetrahydrofolate DehydrogenaseDiabetes Mellitus Type 1EndocrinologyHeptanoic AcidsHMG-CoA reductaseNADPH Oxidase 1biology.proteinEndothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsCardiology and Cardiovascular MedicineCell Adhesion MoleculesDiabetic Angiopathiesmedicine.drugAtherosclerosis
researchProduct

Myocardial and lymphocytic expression of eNOS and nNOS before and after heart transplantation: Relationship to clinical status

2013

Abstract Aims The present study investigates the expression and clinical relevance of the constitutive NO synthases in heart and peripheral blood mononuclear cells (PBMCs) obtained from heart failure patients. Main methods mRNA and protein levels (qRT-PCR and immunoblot) of eNOS and nNOS were determined in: i) Left ventricle (LV, n = 4) and PBMCs (n = 10) from healthy donors; ii) LV, right ventricle (RV) and PBMCs of heart failure (HF) patients (n = 32); and iii) biopsies and PBMCs of the HF patients after cardiac transplant (n = 15). Key findings Expression of constitutive NOS isoforms in heart exhibits wide variability in HF patients, but this variability was not related to aetiology, dis…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIHeart Ventriclesmedicine.medical_treatmentCardiac indexNitric Oxide Synthase Type IPeripheral blood mononuclear cellGeneral Biochemistry Genetics and Molecular BiologyPredictive Value of TestsEnosInternal medicinemedicineHumansClinical significanceGeneral Pharmacology Toxicology and PharmaceuticsHeart FailureHeart transplantationbiologybusiness.industryGeneral MedicineMiddle Agedmedicine.diseasebiology.organism_classificationPulmonary hypertensionmedicine.anatomical_structureVentricleHeart failureLeukocytes MononuclearCardiologyHeart TransplantationFemalebusinessLife Sciences
researchProduct

Chronic Therapy With Isosorbide-5-Mononitrate Causes Endothelial Dysfunction, Oxidative Stress and a Marked Increase in Vascular Endothelin-1 Express…

2011

Aims Isosorbide-5-mononitrate (ISMN) is one of the most frequently used compounds in the treatment of coronary artery disease predominantly in the USA. However, ISMN was reported to induce endothelial dysfunction, which was corrected by vitamin C pointing to a crucial role of reactive oxygen species (ROS) in causing this phenomenon. We sought to elucidate the mechanism how ISMN causes endothelial dysfunction and oxidative stress in vascular tissue. Methods and results Male Wistar rats ( n = 69 in total) were treated with ISMN (75 mg/kg/day) or placebo for 7 days. Endothelin (ET) expression was determined by immunohistochemistry in aortic sections. Isosorbide-5-mononitrate infusion caused si…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIIsosorbide DinitratePharmacologymedicine.disease_causeBiochemistryMicechemistry.chemical_compoundSuperoxidesEnosInternal medicinePhysiology (medical)medicineAnimalsNitric Oxide DonorsEnzyme InhibitorsRats WistarEndothelial dysfunctionCyclic GMPAortaMice KnockoutNADPH oxidaseEndothelin-1biologybusiness.industryNADPH Oxidasesmedicine.diseasebiology.organism_classificationEndothelin 1BosentanRatsNitric oxide synthaseEndothelial stem cellOxidative StressNG-Nitroarginine Methyl EsterEndocrinologychemistryApocyninbiology.proteinEndothelium VascularCardiology and Cardiovascular MedicineEndothelin receptorbusinessOxidative stressSignal Transductionmedicine.drugFree Radical Biology and Medicine
researchProduct

GABAergic inhibition of nitric oxide-mediated relaxation of guinea-pig ileum

1999

The effects of GABA receptor agonists were investigated on guinea-pig isolated ileum longitudinal muscle with intact myenteric plexus. Electrical field stimulation (1 Hz, 10 s) of the histamine (1 microM)-precontracted preparation caused a contraction followed by a relaxation. Relaxations were inhibited by L-N(G)-nitroarginine (L-NA; EC50 3 microM) in a concentration-dependent manner. The inhibitory action of 10 microM L-NA was blocked by 10 microM L-arginine but not by D-arginine, which indicates that the relaxation was largely mediated by endogenous nitric oxide (NO). Tetrodotoxin (1 microM) reduced the relaxation only by about 50%. GABA and the GABA(B) agonist, baclofen, inhibited the fi…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIMuscle RelaxationGuinea PigsTetrodotoxinIn Vitro TechniquesGABAB receptorBicucullineNitric OxideNitroargininechemistry.chemical_compoundGABA receptorIleumInternal medicinemedicineAnimalsGABA-A Receptor AgonistsEnzyme InhibitorsGABA Agonistsgamma-Aminobutyric AcidMyenteric plexusPharmacologyMuscimolGABAA receptorMuscle SmoothGeneral MedicineBicucullineElectric StimulationBaclofenEndocrinologynervous systemchemistryMuscimolGABA-B Receptor AgonistsSaclofenBiophysicsFemaleNitric Oxide SynthaseHistaminemedicine.drugNaunyn-Schmiedeberg's Archives of Pharmacology
researchProduct

Modulation by NO of acetylcholine release in the ileum of wild-type and NOS gene knockout mice.

2002

Nitric oxide (NO) inhibits the release of acetylcholine and cholinergic contractions in the small intestine of several species, but no information is available about the mouse ileum. This study examines the effects of NO on the electrically evoked release of [3H]acetylcholine and smooth muscle contraction in myenteric plexus-longitudinal muscle preparations of wild-type mice and of neuronal NO synthase (nNOS) and endothelial NOS (eNOS) knockout mice. The NOS inhibitor N G-nitro-l-arginine (l-NNA) and the guanylyl cyclase inhibitor 1 H-[1,2,4]oxadiazolo[4,3-α]quinoxalin-1-one (ODQ) concentration dependently increased the evoked [3H]acetylcholine release and cholinergic contractions in prepa…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIPhysiologyNitric Oxide Synthase Type IIIleumNitric Oxide Synthase Type IBiologyIn Vitro TechniquesNitric OxideNitroarginineNitric oxidechemistry.chemical_compoundMiceIleumPhysiology (medical)Internal medicineQuinoxalinesmedicineAnimalsNitric Oxide DonorsEnzyme InhibitorsGene knockoutMice KnockoutOxadiazolesHepatologyPenicillamineGastroenterologyNitric Oxide Synthase Type IIISmall intestineAcetylcholineElectric StimulationNitric oxide synthaseEndocrinologymedicine.anatomical_structurechemistrybiology.proteinCholinergicNitric Oxide SynthaseGastrointestinal MotilityAcetylcholinemedicine.drugAmerican journal of physiology. Gastrointestinal and liver physiology
researchProduct

Resveratrol Reverses Endothelial Nitric-Oxide Synthase Uncoupling in Apolipoprotein E Knockout Mice

2010

A crucial cause of the decreased bioactivity of nitric oxide (NO) in cardiovascular diseases is the uncoupling of the endothelial NO synthase (eNOS) caused by the oxidative stress-mediated deficiency of the NOS cofactor tetrahydrobiopterin (BH(4)). The reversal of eNOS uncoupling might represent a novel therapeutic approach. The treatment of apolipoprotein E knockout (ApoE-KO) mice with resveratrol resulted in the up-regulation of superoxide dismutase (SOD) isoforms (SOD1-SOD3), glutathione peroxidase 1 (GPx1), and catalase and the down-regulation of NADPH oxidases NOX2 and NOX4 in the hearts of ApoE-KO mice. This was associated with reductions in superoxide, 3-nitrotyrosine, and malondiald…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIISOD3SOD2ResveratrolAntioxidantsSuperoxide dismutaseMicechemistry.chemical_compoundApolipoproteins ESuperoxidesEnosMalondialdehydeInternal medicineStilbenesmedicineAnimalsGTP CyclohydrolaseMice KnockoutPharmacologychemistry.chemical_classificationReactive oxygen speciesbiologyReverse Transcriptase Polymerase Chain ReactionSuperoxide DismutaseChemistrySuperoxideMyocardiumTetrahydrobiopterinbiology.organism_classificationBiopterinIsoenzymesOxidative StressEndocrinologyBiochemistryResveratrolbiology.proteinRNATyrosineMolecular Medicinemedicine.drugJournal of Pharmacology and Experimental Therapeutics
researchProduct