Search results for "VASODILATION"

showing 10 items of 228 documents

β-Adrenoceptors differentially regulate vascular tone and angiogenesis of rat aorta via ERK1/2 and p38

2014

β-Adrenoceptors (β-ARs) modulate ERK1/2 and p38 in different cells, but little is known about the contribution of these signaling pathways to the function of β-ARs in vascular tissue. Immunoblotting analysis of rat aortic rings, primary endothelial (ECs) and smooth muscle cells (SMCs) isolated from aorta showed that β-AR stimulation with isoprenaline activated p38 in aortic rings and in both cultured cell types, whereas it had a dual effect on ERK1/2 phosphorylation, decreasing it in ECs while increasing it in SMCs. These effects were reversed by propranolol, which by itself increased p-ERK1/2 in ECs. Isoprenaline β-AR mediated vasodilation of aortic rings was potentiated by the ERK1/2 inhi…

Malemedicine.medical_specialtyEndotheliumPhysiologyAngiogenesisVasodilator AgentsAdrenergic beta-AntagonistsMyocytes Smooth MuscleNeovascularization PhysiologicAorta ThoracicStimulationVasodilationFibroblast growth factorp38 Mitogen-Activated Protein KinasesMuscle Smooth VascularInternal medicineIsoprenalinemedicine.arteryReceptors Adrenergic betamedicineAnimalsHumansRats WistarMitogen-Activated Protein Kinase 1PharmacologyMatrigelAortaMitogen-Activated Protein Kinase 3business.industryAdrenergic beta-AgonistsPropranololRatsVasodilationHEK293 Cellsmedicine.anatomical_structureEndocrinologycardiovascular systemMolecular MedicineEndothelium Vascularbusinessmedicine.drugVascular Pharmacology
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Elevation of plasma viscosity induces sustained NO-mediated dilation in the hamster cremaster microcirculation in vivo

1997

We studied whether a flow-independent increase of luminal wall shear stress (WSS) could dilate hamster arterioles in vivo and which endothelial mediators are potentially involved. To this end the plasma viscosity was elevated by exchanging blood for dextran-erythrocyte solution thereby augmenting WSS. Diameters of small and large arterioles as well as red blood cell velocities were measured before and after exchange of blood for solutions of identical haematocrit containing either high- (HMWD) or low-molecular weight dextran (LMWD). The potential role of endothelial autacoids was investigated by local application of the NO-synthase inhibitor NG-nitro-L-arginine (L-NNA), the inhibitor of cyc…

Malemedicine.medical_specialtyEndotheliumPhysiologyClinical BiochemistryPlasma SubstitutesHamsterGenitalia MaleNitric OxideMicrocirculationPlasmachemistry.chemical_compoundIn vivoCricetinaePhysiology (medical)Internal medicinePotassium Channel BlockersmedicineAnimalsBlood TransfusionCyclooxygenase InhibitorsMesocricetusMusclesDextransAnatomyBlood ViscosityMolecular WeightVasodilationArteriolesRed blood cellDextranmedicine.anatomical_structureEndocrinologychemistrycardiovascular systemDilation (morphology)Stress MechanicalNitric Oxide SynthaseErythrocyte TransfusionAutacoidcirculatory and respiratory physiologyPfl�gers Archiv European Journal of Physiology
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Serum alkaline phosphatase negatively affects endothelium-dependent vasodilation in naïve hypertensive patients.

2015

Tissue nonspecific alkaline phosphatase, promoting arterial calcification in experimental models, is a powerful predictor of total and cardiovascular mortality in general population and in patients with renal or cardiovascular diseases. For this study, to evaluate a possible correlation between serum alkaline phosphatase levels and endothelial function, assessed by strain gauge plethysmography, we enrolled 500 naïve hypertensives divided into increasing tertiles of alkaline phosphatase. The maximal response to acetylcholine was inversely related to alkaline phosphatase ( r =−0.55; P <0.001), and this association was independent ( r =−0.61; P <0.001) of demographic and classical risk …

Malemedicine.medical_specialtyEndotheliumPopulationRenal functionchemistry.chemical_elementVasodilationCalciumFollow-Up StudieatherosclerosiRisk FactorsInternal medicineInternal MedicinemedicineHumansEndothelial dysfunctioneducationriskeducation.field_of_studybusiness.industryRisk FactorMedicine (all)IncidenceMiddle Agedmedicine.diseaseAlkaline PhosphataseacetylcholinePlethysmographyVasodilationmedicine.anatomical_structureEndocrinologychemistryItalyHypertensionAlbuminuriaAlkaline phosphataseFemaleacetylcholine; alkaline phosphatase; atherosclerosis; hypertension; riskEndothelium Vascularatherosclerosismedicine.symptombusinessHumanFollow-Up StudiesHypertension (Dallas, Tex. : 1979)
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Mechanisms underlying the diabetes-induced hyporeactivity of the rabbit carotid artery to atrial natriuretic peptide

2010

Abstract Atrial natriuretic peptide (ANP) plays an important role in the pathophysiology of the vascular complications in diabetes. The working hypothesis was that diabetes might modify the vascular actions of ANP in isolated rabbit carotid arteries and the mechanisms involved in these actions. ANP (10 −12 –10 −7  M) induced a relaxation of precontracted carotid arteries, which was lower in diabetic than in control rabbits. In arteries from both groups of animals, endothelium removal increased the ANP-induced relaxation. Isatin inhibited the relaxation to ANP both in arteries with and without endothelium. Carotid arteries from diabetic rabbits showed a decreased natriuretic peptide receptor…

Malemedicine.medical_specialtyEndotheliummedicine.drug_classThromboxaneDown-RegulationProstacyclinVasodilationDiabetes Mellitus ExperimentalRandom AllocationAtrial natriuretic peptideDiabetes mellitusInternal medicinemedicineNatriuretic peptideAnimalsReceptorPharmacologybusiness.industrymedicine.diseaseVasodilationCarotid Arteriesmedicine.anatomical_structureEndocrinologycardiovascular systemRabbitsbusinessAtrial Natriuretic Factorhormones hormone substitutes and hormone antagonistscirculatory and respiratory physiologymedicine.drugPharmacological Research
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Nail fold capillary diameter changes in acute systemic hypoxia.

2013

The present study was undertaken to determine the effect of arterial blood hypoxemia induced by acute systemic hypoxia (pO2=12%) on capillary recruitment and diameter, and red blood cell (RBC) velocity in human nail fold capillaries during rest, arterial post-occlusive reactive hyperemia (PRH), and venous occlusion (VO) using intravital video-capillaroscopy. Capillary recruitment was unchanged in acute systemic hypoxia (H) versus normoxia (N). There was no difference in RBC velocity measurements between normoxia and hypoxia (P<0.63). However, a statistically significant increase in nail fold capillary total width (N, 39.9±9.1 vs. H, 42.7±10.3 μm; P<0.05), apical diameter (N, 15.5±4.3 vs. H,…

Malemedicine.medical_specialtyErythrocytesVideo RecordingVasodilationHyperemiaBiochemistryHypoxemiaMicrocirculationMicroscopic AngioscopyYoung AdultInternal medicinemedicineHumansHypoxiaReactive hyperemiabusiness.industryMicrocirculationCell BiologyBlood flowHypoxia (medical)CapillariesVasodilationRed blood cellmedicine.anatomical_structureNailsRegional Blood FlowAnesthesiaCardiologyArterial bloodFemalemedicine.symptomCardiology and Cardiovascular MedicinebusinessBlood Flow VelocityMicrovascular research
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Maternal Treatment of Spontaneously Hypertensive Rats With Pentaerythritol Tetranitrate Reduces Blood Pressure in Female Offspring

2014

Pentaerythritol tetranitrate is devoid of nitrate tolerance and shows no reproductive or developmental toxicity in animal studies. Recently, pentaerythritol tetranitrate has been demonstrated to reduce the risk of intrauterine growth restriction and the risk of preterm birth in women with abnormal placental perfusion. This study was conducted to test the perinatal programming effect of pentaerythritol tetranitrate in spontaneously hypertensive rats, a rat model of genetic hypertension. Parental spontaneously hypertensive rats were treated with pentaerythritol tetranitrate (50 mg/kg per day) during pregnancy and lactation periods; the offspring received standard chow without pentaerythritol …

Malemedicine.medical_specialtyGPX1Nitric Oxide Synthase Type IIIOffspringVasodilator AgentsDevelopmental toxicityBlood PressureVasodilationPentaerythritol tetranitratePentaerythritolchemistry.chemical_compoundPregnancyRats Inbred SHRInternal medicineInternal MedicinemedicineAnimalsPentaerythritol Tetranitratebusiness.industryGene Expression Regulation DevelopmentalDNARatsVasodilationHeme oxygenaseEndocrinologyBlood pressureAnimals NewbornchemistryMaternal ExposureHypertensionPregnancy AnimalFemaleEndothelium VascularbusinessHypertension
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Elevated levels of asymmetric dimethylarginine in chronic heart failure: a pathophysiologic link between oxygen radical load and impaired vasodilator…

2010

Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide-dependent vasodilation. In 113 patients with chronic heart failure (CHF) and 26 controls, ADMA level was studied in relation to peripheral blood flow and vasodilator capacity. Further, the effects of allopurinol on concentrations of reactive oxygen species (ROS) and ADMA and peripheral vasodilator capacity were tested in a double-blind design. ADMA level was found to be elevated in CHF patients as compared with controls and increased in parallel with New York Heart Association (NYHA) class and exercise capacity (all P < 0.0001). The level of ADMA predicted resting blood flow (P < 0.05) and postischemic vasodilator…

Malemedicine.medical_specialtyHeart diseaseAllopurinolAllopurinolheart failureVasodilationmedicine.disease_causeArgininechemistry.chemical_compoundDouble-Blind Methodendothelial functionInternal medicineMedicineHumansoxidative stressPharmacology (medical)Xanthine oxidaseAgedPharmacologybusiness.industryFree Radical ScavengersMiddle Agedmedicine.diseaseUric AcidVasodilationEndocrinologyCross-Sectional Studieschemistryheart failure; oxidative stress; endothelial functionHeart failureChronic DiseaseUric acidCitrullineFemalebusinessAsymmetric dimethylarginineReactive Oxygen SpeciesOxidative stressmedicine.drug
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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
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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
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Oxidative Inhibition of the Mitochondrial Aldehyde Dehydrogenase Promotes Nitroglycerin Tolerance in Human Blood Vessels

2007

Objectives We tested the hypothesis of whether an inhibition of the nitroglycerin (GTN) bioactivating enzyme mitochondrial aldehyde dehydrogenase (ALDH-2) contributes to GTN tolerance in human blood vessels. Background The hemodynamic effects of GTN are rapidly blunted by the development of tolerance, a phenomenon associated with increased formation of reactive oxygen species (ROS). Recent studies suggest that ROS-induced inhibition of ALDH-2 accounts for tolerance in animal models. Methods Segments of surgically removed arteria mammaria and vena saphena from patients undergoing coronary bypass surgery were used to examine the vascular responsiveness to GTN and the endothelium-dependent vas…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIVasodilator AgentsMyocardial InfarctionAldehyde dehydrogenaseVasodilationPharmacologyDrug Administration ScheduleTissue Culture TechniquesNitroglycerinIn vivoEnosmedicineHumansSaphenous VeinEndothelial dysfunctionMammary ArteriesAgedbiologybusiness.industryAldehyde Dehydrogenase MitochondrialDrug ToleranceAldehyde Dehydrogenasemedicine.diseasebiology.organism_classificationAcetylcholineSurgeryOxidative Stressmedicine.anatomical_structureCirculatory systemcardiovascular systembiology.proteinFemaleAnimal studiesbusinessCardiology and Cardiovascular Medicinecirculatory and respiratory physiologyBlood vesselJournal of the American College of Cardiology
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