Search results for "dilation"

showing 10 items of 304 documents

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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Sum of ST-segment elevations on admission electrocardiograms in acute myocardial infarction predicts left ventricular dilation.

1996

In summary, ST-segment elevations on the admission electrocardiogram not only diagnose acute myocardial infarction but also provide predictive information with respect to developing infarct size and left ventricular remodeling as well as survival.

Malemedicine.medical_specialtyLeft ventricular dilationHeart VentriclesMyocardial InfarctionElectrocardiographyPatient AdmissionPredictive Value of TestsRisk FactorsInternal medicinemedicineST segmentHumanscardiovascular diseasesMyocardial infarctionVentricular remodelingAgedmedicine.diagnostic_testbusiness.industryST elevationMyocardiumElectrocardiography in myocardial infarctionMiddle Agedmedicine.diseasePredictive value of testscardiovascular systemCardiologyFemaleHypertrophy Left VentricularCardiology and Cardiovascular MedicinebusinessElectrocardiographyThe American journal of cardiology
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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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Relaxant effect of sildenafil in the rabbit basilar artery

2005

We hypothesized that sildenafil, inhibitor of phosphodiesterase-5 (PDE-5), interacts with the nitric oxide (NO)-cGMP pathway in the cerebral arteries and shows vasoactive effects. To prove it in the isolated rabbit basilar artery, we compared the effects of sildenafil with other PDE-5 inhibitors, assessed the endothelial dependence of the vasoactive responses, and used modulators of the cGMP and cAMP signaling processes. Sildenafil (10 nM-0.1 mM) induced concentration-dependent relaxations of endothelin-1 (10 nM)-precontracted basilar artery, which were partially inhibited both in endothelium-denuded arteries and in arteries precontracted by depolarization with KCl (50 mM). Endothelin-1 (1 …

Malemedicine.medical_specialtyPhosphodiesterase InhibitorsPhysiologySildenafilVasodilator AgentsCerebral arteriesVasodilationIn Vitro TechniquesPiperazinesSildenafil Citratechemistry.chemical_compound3'5'-Cyclic-GMP PhosphodiesterasesQuinoxalinesmedicine.arteryInternal medicinemedicineBasilar arteryAnimalsSulfonesCyclic Nucleotide Phosphodiesterases Type 5PharmacologyOxadiazolesDose-Response Relationship DrugPhosphoric Diester HydrolasesPDE5 drug designVasodilationNG-Nitroarginine Methyl EsterEndocrinologychemistryGuanylate CyclasePurinesBasilar Arterycardiovascular systemMolecular MedicineRabbitsSodium nitroprussideNitric Oxide SynthaseSoluble guanylyl cyclaseZaprinastSignal Transductionmedicine.drugVascular Pharmacology
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Diabetes impairs the atrial natriuretic peptide relaxant action mediated by potassium channels and prostacyclin in the rabbit renal artery.

2012

Diabetes is associated with increased prevalence of hypertension, cardiovascular and renal disease. Atrial natriuretic peptide (ANP) plays an important role in cardiovascular pathophysiology and is claimed to have cardioprotective and renoprotective effect in diabetic patients. The working hypothesis was that alloxan-induced diabetes might modify the vascular effects of ANP in isolated rabbit renal arteries and the mechanisms involved in such actions. Plasma ANP levels were higher in diabetic rabbits than in control rabbits. ANP (10(-12)-10(-7)M) induced a relaxation of precontracted renal arteries, which was lower in diabetic than in control rabbits. In arteries from both groups of animals…

Malemedicine.medical_specialtyPotassium ChannelsEndotheliumProstacyclinIn Vitro TechniquesDiabetes Mellitus ExperimentalGlibenclamideThromboxane A2chemistry.chemical_compoundThromboxane A2Renal ArteryAtrial natriuretic peptidemedicine.arteryDiabetes mellitusInternal medicinemedicineAnimalsRenal arteryPharmacologybusiness.industryTetraethylammoniummedicine.diseaseEpoprostenolPotassium channelVasodilationEndocrinologymedicine.anatomical_structurechemistrycardiovascular systemEndothelium VascularRabbitsbusinesshormones hormone substitutes and hormone antagonistsAtrial Natriuretic Factorcirculatory and respiratory physiologymedicine.drugPharmacological research
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