Search results for "VASODILATION"

showing 10 items of 228 documents

4-Hydroxynonenal, a lipid peroxidation product, induces relaxation of human cerebral arteries.

1994

The relaxant effect of 4-hydroxynonenal (4-HNE), a lipid peroxidation product, on human cerebral arteries was studied. Addition of 4-HNE to artery rings promoted no contraction, and after stimulation with prostaglandin F2α (PFG2α; 10−7-3 × 10−6 M), 100% relaxation was obtained with 3 × 10−5 M 4-HNE. Inhibition of nitric oxide formation with NG-nitro-l-arginine methyl ester hydrochloride (l-NAME; (10−4 M), as well as prostaglandin synthesis with indomethacin (3 × 10−6 M), partially prevented 4-HNE-induced relaxation, but each of these substances separately failed to inhibit complete relaxation. Addition of both inhibitors together reduced 4-HNE-induced relaxation to ≈50%, but relaxation cou…

MaleLipid PeroxidesContraction (grammar)EndotheliumIndomethacinCerebral arteriesStimulationVasodilationArginineDinoprostNitric Oxide4-HydroxynonenalNitric oxideLipid peroxidationchemistry.chemical_compoundCadavermedicineHumansAgedAged 80 and overAldehydesDose-Response Relationship DrugChemistryOsmolar ConcentrationCerebral ArteriesMiddle AgedVasodilationNG-Nitroarginine Methyl Estermedicine.anatomical_structureNeurologyBiochemistryBiophysicsEndothelium VascularNeurology (clinical)Cardiology and Cardiovascular Medicine
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Early Cellular Reactions in Mechanically Stimulated Gingival Connective Tissue

2001

Aim: The aim of this study was to describe early cellular reactions occuring in mechnically stimulated gingival connective tissue. Material and Method: Elastic bands were inserted between the maxillary first and second molars of male rats aged 8 weeks, which were pulse-labeled with 3H-thymidine and subsequently killed in groups together with labeled control animals after periods of 1–168 hours. Autoradiographs were prepared from plastic mesiodistal sections and parameters of cell proliferation determined in gingival connective tissue sampling areas coronal to the interdental bone crest and in the central zone of the body of the papilla between the second and third molars. The incidence of m…

MaleMolarPathologymedicine.medical_specialtyTooth Movement TechniquesEndotheliumGingivaConnective tissueOrthodonticsStimulationMandibular second molarmedicineAnimalsEndotheliumFibroblastbusiness.industryMacrophagesRats Inbred StrainsFibroblastsMolarRatsVasodilationMajor duodenal papillaEndothelial stem cellmedicine.anatomical_structureConnective TissueOral SurgerybusinessCell DivisionJournal of Orofacial Orthopedics/Fortschritte der Kieferorthop�die
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Monitoring White Blood Cell Mitochondrial Aldehyde Dehydrogenase Activity: Implications for Nitrate Therapy in Humans

2009

Recent animal data suggest that reduced lipoic acid (LA) prevents oxidative inhibition of the nitrate bioactivating enzyme, the mitochondrial aldehyde dehydrogenase (ALDH-2), and that pentaerythritol tetranitrate (PETN) does not induce nitrate tolerance because of its intrinsic antioxidative properties, thereby preserving ALDH-2 activity. We sought to determine whether ALDH-2 activity in circulating white blood cells (WBCs) can be used to monitor nitrate tolerance and whether LA can prevent nitroglycerin tachyphylaxis in humans. Eight healthy male volunteers received, in randomized order, a single dose of glyceryl trinitrate (GTN; 0.8 mg), PETN (80 mg), or GTN plus LA (600 mg) orally. GTN (…

MaleMyocardial IschemiaAldehyde dehydrogenasePentaerythritol tetranitrateVasodilationTachyphylaxisPharmacologymedicine.disease_causeMitochondria Heartchemistry.chemical_compoundAnimal dataWhite blood cellLeukocytesmedicineAnimalsHumansRats WistarPharmacologyNitratesbiologyAldehyde DehydrogenaseRatsEnzyme ActivationVasodilationLipoic acidmedicine.anatomical_structurechemistrybiology.proteinMolecular MedicineOxidative stresscirculatory and respiratory physiologyJournal of Pharmacology and Experimental Therapeutics
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Nitroglycerin-induced endothelial dysfunction and tolerance involve adverse phosphorylation and S-glutathionylation of endothelial nitric oxide synth…

2011

Continuous administration of nitroglycerin (GTN) causes tolerance and endothelial dysfunction by inducing reactive oxygen species (ROS) production from various enzymatic sources, such as mitochondria, NADPH oxidase, and an uncoupled endothelial nitric oxide synthase (eNOS). In the present study, we tested the effects of type 1 angiotensin (AT(1))-receptor blockade with telmisartan on GTN-induced endothelial dysfunction in particular on eNOS phosphorylation and S-glutathionylation sites and the eNOS cofactor synthesizing enzyme GTP-cyclohydrolase I.Wistar rats were treated with telmisartan (2.7 or 8 mg/kg per day PO for 10 days) and with GTN (50 mg/kg per day SC for 3 days). Aortic eNOS phos…

MaleNitric Oxide Synthase Type IIIPhysiologyVasodilator AgentsPharmacologyBenzoatesCell LineNitroglycerinmedicineAnimalsHumansTelmisartanEnzyme InhibitorsPhosphorylationRats WistarS-GlutathionylationEndothelial dysfunctionGTP CyclohydrolaseBeneficial effectsNitroglycerinPharmacologyAngiotensin II receptor type 1Dose-Response Relationship DrugEndothelial nitric oxide synthaseChemistryEndothelial CellsDrug ToleranceAldehyde Dehydrogenasemedicine.diseaseGlutathioneMitochondriaRatsVasodilationOxidative StressTetrahydrofolate DehydrogenaseMolecular MedicinePhosphorylationBenzimidazolesEndothelium VascularTelmisartanReactive Oxygen SpeciesAngiotensin II Type 1 Receptor BlockersProtein Processing Post-Translationalmedicine.drugVascular Pharmacology
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Diabetes potentiates acetylcholine-induced relaxation in rabbit renal arteries.

2001

Abstract The response of rabbit renal arteries to acetylcholine and its endothelial modulation in diabetes were investigated. Acetylcholine induced concentration-related endothelium-dependent relaxation of renal arteries that was significantly more potent in diabetic rabbits than in control rabbits. Pretreatment with NG-nitro- l -arginine ( l -NOArg), indomethacin, or l -NOArg plus indomethacin induced partial inhibition of acetylcholine-induced relaxation. Inhibition induced by l -NOArg plus indomethacin was significantly higher in arteries from diabetic rabbits than in arteries from control rabbits. In renal arteries depolarised with KCl 30 mM and incubated with l -NOArg plus indomethacin…

MaleNitroprussidemedicine.medical_specialtyArginineEndotheliumVasodilator AgentsIndomethacinProstacyclinNitric OxideNitroarginineNitric oxideDiabetes Mellitus Experimentalchemistry.chemical_compoundRenal Arterymedicine.arteryInternal medicineMedicineAnimalsRenal arteryEnzyme InhibitorsPharmacologybusiness.industryAnti-Inflammatory Agents Non-SteroidalAcetylcholineVasodilationEndocrinologymedicine.anatomical_structurechemistrycardiovascular systemSodium nitroprussideEndothelium VascularRabbitsbusinessAcetylcholinemedicine.drugArteryEuropean journal of pharmacology
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Cholinergic Responses of Ophthalmic Arteries in M3and M5Muscarinic Acetylcholine Receptor Knockout Mice

2009

PURPOSE. To determine the functional role of M 3 and M 5 muscarinic acetylcholine receptor subtypes in ophthalmic arteries using gene-targeted mice. METHODS. Muscarinic receptor gene expression was quantified in murine ophthalmic arteries using real-time PCR. To test the functional relevance of M 3 and M 5 receptors, ophthalmic arteries from mice deficient in either subtype (M3R -/- , M5R -/- , respectively) and wild-type controls were isolated, cannulated with micropipettes, and pressurized. Changes in luminal vessel diameter in response to muscarinic and nonmuscarinic receptor agonists were measured by video microscopy. RESULTS. With the use of real-time PCR, all five muscarinic receptor …

MaleNitroprussidemedicine.medical_specialtyCarbacholVasodilator AgentsCholinergic AgentsVideo RecordingGene ExpressionBiologyBradykininArticleMiceOphthalmic ArteryPhenylephrineInternal medicineMuscarinic acetylcholine receptorMuscarinic acetylcholine receptor M4medicineAnimalsRNA MessengerMice KnockoutReceptor Muscarinic M3Receptor Muscarinic M5Reverse Transcriptase Polymerase Chain ReactionMuscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2Muscarinic acetylcholine receptor M1AcetylcholineVasodilationEndocrinologyCholinergicCarbacholAdrenergic alpha-AgonistsAcetylcholinemedicine.drugInvestigative Opthalmology & Visual Science
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Identification of the Muscarinic Acetylcholine Receptor Subtype Mediating Cholinergic Vasodilation in Murine Retinal Arterioles

2011

To identify the muscarinic acetylcholine receptor subtype that mediates cholinergic vasodilation in murine retinal arterioles.Muscarinic receptor gene expression was determined in murine retinal arterioles using real-time PCR. To assess the functional relevance of muscarinic receptors for mediating vascular responses, retinal vascular preparations from muscarinic receptor-deficient mice were studied in vitro. Changes in luminal arteriole diameter in response to muscarinic and nonmuscarinic vasoactive substances were measured by video microscopy.Only mRNA for the M(3) receptor was detected in retinal arterioles. Thus, M(3) receptor-deficient mice (M3R(-/-)) and respective wild-type controls …

MaleNitroprussidemedicine.medical_specialtyNitric Oxide Synthase Type IIIRetinal ArteryVideo RecordingGene ExpressionBiologyReal-Time Polymerase Chain ReactionMuscle Smooth VascularMiceInternal medicineMuscarinic acetylcholine receptor M5Muscarinic acetylcholine receptormedicineMuscarinic acetylcholine receptor M4AnimalsRNA MessengerMice KnockoutReceptor Muscarinic M3Dose-Response Relationship DrugMuscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2ArticlesMuscarinic acetylcholine receptor M1AcetylcholineVasodilationArteriolesNG-Nitroarginine Methyl EsterEndocrinologyCholinergicCarbacholFemaleEndothelium VascularAcetylcholinemedicine.drugInvestigative Opthalmology & Visual Science
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Contribution of nitric oxide synthase isoforms to cholinergic vasodilation in murine retinal arterioles.

2013

Abstract Nitric oxide synthases (NOSs) are critically involved in regulation of ocular perfusion. However, the contribution of the individual NOS isoforms to vascular responses is unknown in the retina. Because some previous findings suggested an involvement of inducible nitric oxide synthase (iNOS) in the regulation of retinal vascular tone, a major goal of the present study was to examine the hypothesis that iNOS is involved in mediating cholinergic vasodilation responses of murine retinal arterioles. Another subject of this study was to test the contribution of the other two NOS isoforms, neuronal (nNOS) and endothelial NOS (eNOS), to cholinergic retinal arteriole responses. Expression o…

MaleNitroprussidemedicine.medical_specialtyNitric Oxide Synthase Type IIIVasodilator AgentsNitric Oxide Synthase Type IIVasodilationNitric Oxide Synthase Type IBiologyEndothelial NOSReal-Time Polymerase Chain ReactionGene Expression Regulation EnzymologicNitric oxideCellular and Molecular Neurosciencechemistry.chemical_compoundMiceInternal medicinemedicineAnimalsRNA MessengerEnzyme InhibitorsMice KnockoutBrainRetinal VesselsRetinalSensory SystemsAcetylcholineNitric oxide synthaseMice Inbred C57BLVasodilationOphthalmologyArteriolesEndocrinologyNG-Nitroarginine Methyl Esterchemistrybiology.proteinCholinergicmedicine.symptomVasoconstrictionAcetylcholinemedicine.drugExperimental eye research
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Role of M1, M3, and M5 muscarinic acetylcholine receptors in cholinergic dilation of small arteries studied with gene-targeted mice

2011

Acetylcholine regulates perfusion of numerous organs via changes in local blood flow involving muscarinic receptor-induced release of vasorelaxing agents from the endothelium. The purpose of the present study was to determine the role of M1, M3, and M5 muscarinic acetylcholine receptors in vasodilation of small arteries using gene-targeted mice deficient in either of the three receptor subtypes (M1R−/−, M3R−/−, or M5R−/− mice, respectively). Muscarinic receptor gene expression was determined in murine cutaneous, skeletal muscle, and renal interlobar arteries using real-time PCR. Moreover, respective arteries from M1R−/−, M3R−/−, M5R−/−, and wild-type mice were isolated, cannulated with mic…

MaleNitroprussidemedicine.medical_specialtyPhysiologyVasodilator AgentsVascular Biology and MicrocirculationSubstance PBiologyKidneyMicePhysiology (medical)Internal medicineMuscarinic acetylcholine receptormedicineAnimalsRNA MessengerMuscle SkeletalSkinAcetylcholine receptorMice KnockoutReceptor Muscarinic M3Receptor Muscarinic M5Dose-Response Relationship DrugReceptor Muscarinic M1Muscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2ArteriesMuscarinic acetylcholine receptor M1Interlobar arteriesAcetylcholineVasodilationmedicine.anatomical_structureEndocrinologyModels AnimalCholinergicCardiology and Cardiovascular MedicineAcetylcholinemedicine.drugAmerican Journal of Physiology-Heart and Circulatory Physiology
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Ca2+-activated K+ channels mediate relaxation of forearm veins in chronic renal failure

2003

In arteries, agonists such as acetylcholine release an endothelium-derived hyperpolarizing factor (EDHF) that is neither nitric oxide nor prostacyclin.To examine the responses to acetylcholine in segments of forearm veins from patients with chronic renal failure who either had never received dialysis or had undergone long-term dialysis, and to determine the contribution of nitric oxide and EDHF to endothelium-dependent relaxation in veins from patients with chronic renal failure.Isometric tension was recorded in rings of forearm vein from 34 non-dialysed patients, 27 dialysed patients and 14 multiorgan donors (controls).Relaxation in response to acetylcholine was reduced in veins of non-dia…

MaleNitroprussidemedicine.medical_specialtyPhysiologyVasodilator AgentsVasodilationIn Vitro TechniquesNitric OxideVeinsNitric oxideBiological FactorsPotassium Channels Calcium-Activatedchemistry.chemical_compoundForearmQuinoxalinesInternal medicineInternal MedicinemedicineHumansEnzyme InhibitorsVeinOxadiazolesomega-N-MethylarginineVascular diseasebusiness.industryMiddle Agedmedicine.diseaseAcetylcholinePotassium channelVasodilationForearmEndocrinologymedicine.anatomical_structurechemistrycardiovascular systemKidney Failure ChronicFemaleNitric Oxide SynthaseCardiology and Cardiovascular MedicinebusinessAcetylcholineKidney diseasemedicine.drugJournal of Hypertension
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