Search results for "Arteriole"

showing 10 items of 26 documents

Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX 3 CL1) Expression by Angiotensin-II

2012

Objective— Angiotensin-II (Ang-II) promotes the interaction of mononuclear cells with arterioles and neutrophils with postcapillary venules. To investigate the mechanisms underlying this dissimilar response, the involvement of fractalkine (CX 3 CL1) was explored. Methods and Results— Enhanced CX 3 CL1 expression was detected in both cremasteric arterioles and postcapillary venules 24 hours after Ang-II intrascrotal injection. Arteriolar leukocyte adhesion was the unique parameter significantly reduced (83%) in animals lacking CX 3 CL1 receptor (CX 3 CR1). Human umbilical arterial and venous endothelial cell stimulation with 1 μmol/L Ang-II increased CX 3 CL1 expression, yet neutralization …

MalePathologyTime Factorsp38 Mitogen-Activated Protein KinasesMiceVenulesLeukocytesEndothelial dysfunctionExtracellular Signal-Regulated MAP KinasesReceptorCells CulturedMice KnockoutMembrane GlycoproteinsAngiotensin IINF-kappa BArteriesEndothelial stem cellArteriolesNADPH Oxidase 5NADPH Oxidase 4NADPH Oxidase 2FemaleRNA InterferenceReceptors ChemokineTumor necrosis factor alphaCardiology and Cardiovascular MedicineSignal Transductionmedicine.medical_specialtyCX3C Chemokine Receptor 1BiologyTransfectionPeripheral blood mononuclear cellLosartanVeinsInterferon-gammaApolipoproteins EDownregulation and upregulationInternal medicineCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansLeukocyte RollingCX3CL1Chemokine CX3CL1Tumor Necrosis Factor-alphaEndothelial CellsMembrane ProteinsNADPH OxidasesAtherosclerosismedicine.diseaseAngiotensin IIMice Inbred C57BLDisease Models AnimalEndocrinologyAngiotensin II Type 1 Receptor BlockersArteriosclerosis, Thrombosis, and Vascular Biology
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Inflammation-responsive focal constrictors in the mouse ear microcirculation

2006

In many capillary exchange beds, blood flow is locally regulated by precapillary sphincter-like activity. In this study, we used intravascular tracers and scanning electron microscopy to investigate precapillary blood flow regulation in the mouse ear. Gelatin ink injections of the normal mouse ear demonstrated 6.8 +/- 2.3 axial vessels with a cutoff of detectable tracer in the early branches: 19 +/- 11 focal constrictions were observed along the 1st to 5th order branches of the axial vessels. A perfusion tracer consisting of biotinylated anti-endothelial lectins (Ricinus Communis Agglutin, Lycopersicon Esculentum and Griffonia Simplicifolia) was circulated for 30 min under physiological con…

MalePathologymedicine.medical_specialtyHistologyInflammationVasodilationCorrosion CastingMicrocirculationMicechemistry.chemical_compoundVenulesPrecapillary sphinctermedicineAnimalsEar ExternalProstaglandin E1Molecular BiologyEcology Evolution Behavior and SystematicsSkinMice Inbred BALB CbiologyChemistryMicrocirculationGriffonia simplicifoliaOriginal ArticlesCell BiologyAnatomyBlood flowbiology.organism_classificationCapillariesArteriolesErythemaRegional Blood FlowMicroscopy Electron ScanningFemaleAnatomymedicine.symptomPerfusionDevelopmental BiologyJournal of Anatomy
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A critical role for TNFα in the selective attachment of mononuclear leukocytes to angiotensin-II-stimulated arterioles

2007

Abstract Angiotensin II (Ang-II) exerts inflammatory activity and is involved in different cardiovascular disorders. This study has evaluated the involvement of tumor necrosis factor alpha (TNFα) in the leukocyte accumulation elicited by Ang-II. Ang-II (1 nM intraperitoneally in rats) induced TNFα release at 1 hour followed by neutrophil and mononuclear cell recruitment. The administration of an antirat TNFα antiserum had no effect on Ang-IIinduced neutrophil accumulation but inhibited the infiltration of mononuclear cells and reduced CC chemokine content in the peritoneal exudate. Pretreatment with either an anti-TNFα or an anti-IL-4 antiserum decreased Ang-II-induced arteriolar mononuclea…

MaleUmbilical Veinsmedicine.medical_specialtyEndotheliummedicine.medical_treatmentImmunologyBiologyBiochemistryPeripheral blood mononuclear cellMicrocirculationRats Sprague-DawleyInternal medicineCell AdhesionmedicineAnimalsHumansVasoconstrictor AgentsRNA MessengerVenuleReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaAngiotensin IICell BiologyHematologyAngiotensin IIRatsArteriolesMononuclear cell infiltrationmedicine.anatomical_structureCytokineEndocrinologyLeukocytes MononuclearTumor necrosis factor alphaEndothelium VascularInterleukin-4ChemokinesInjections IntraperitonealBlood
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Complement Activation in Peritoneal Dialysis–Induced Arteriolopathy

2017

Cardiovascular disease (CVD) is the leading cause of increased mortality in patients with CKD and is further aggravated by peritoneal dialysis (PD). Children are devoid of preexisting CVD and provide unique insight into specific uremia- and PD-induced pathomechanisms of CVD. We obtained peritoneal specimens from children with stage 5 CKD at time of PD catheter insertion (CKD5 group), children with established PD (PD group), and age-matched nonuremic controls (n=6/group). We microdissected omental arterioles from tissue layers not directly exposed to PD fluid and used adjacent sections of four arterioles per patient for transcriptomic and proteomic analyses. Findings were validated in omenta…

MaleVascular Endothelial Growth Factor A0301 basic medicinePathologyProteomemedicine.medical_treatmentComplement Membrane Attack ComplexSmad2 ProteinSeverity of Illness IndexTransforming Growth Factor betaMedicinePhosphorylationChildComplement ActivationCatheter insertionGeneral MedicineArteriosclerosisArteriolesComplement C3dNephrologyChild PreschoolFemaleOmentumPeritoneal DialysisSignal Transductionmedicine.medical_specialtyAdolescentPeritoneal dialysis03 medical and health sciencesDownregulation and upregulationClinical ResearchTGF beta signaling pathwayHumansSmad3 ProteinVascular DiseasesUremiabusiness.industryVascular diseaseComplement C1qInfant NewbornInfantComplement System Proteinsmedicine.diseaseUremiaComplement systemGene Ontology030104 developmental biologyCase-Control StudiesKidney Failure ChronicTranscriptomebusinessJournal of the American Society of Nephrology
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Direct evidence of leukocyte adhesion in arterioles by angiotensin II

2004

AbstractAlthough leukocytes adhere in arteries in various vascular diseases, to date no endogenous proinflammatory molecule has been identified to initiate leukocyte adhesion in the arterial vasculature. This study was undertaken to assess angiotensin II (Ang II)-induced leukocyte adhesion in arterioles in vivo. Rats received intraperitoneal injections of Ang II; 4 hours later, leukocyte recruitment in mesenteric microcirculation was examined using intravital microscopy. Ang II (1 nM) produced significant arteriolar leukocyte adhesion of mononuclear cells. Using function-blocking monoclonal antibodies (mAbs) against different rat cell adhesion molecules (CAMs), we discovered that this effec…

Malemedicine.medical_specialtyEndotheliumIntegrin alpha4ImmunologyIntercellular Adhesion Molecule-1Vascular Cell Adhesion Molecule-1BiologyBiochemistryRats Sprague-DawleyVenulesInternal medicineCell AdhesionLeukocytesmedicineAnimalsVasoconstrictor AgentsLeukocyte RollingCell adhesionCell adhesion moleculeAngiotensin IINF-kappa BCell BiologyHematologyIntercellular Adhesion Molecule-1Angiotensin IIRatsArteriolesmedicine.anatomical_structureEndocrinologyCD18 AntigensImmunologyEndothelium VascularIntravital microscopySelectinArteryBlood
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Nitric Oxide Opposes Myogenic Pressure Responses Predominantly in Large Arterioles In Vivo

1998

Abstract —A myogenic vasoconstriction may amplify the effects of circulating vasoconstrictors. In cremaster arterioles, the contribution of a myogenic component to the constriction on intravenous infusion of norepinephrine (NE) or angiotensin II (Ang II) was studied. Second, the role of endothelium-derived nitric oxide (NO) in the control of these myogenic constrictions and its site of action in the resistance vascular bed was investigated. In 30 anesthetized (pentobarbital) hamsters, the cremaster was prepared for intravital microscopy, and a pneumatic vessel occluder was placed around the aorta to vary blood pressure in the hindquarter of the animal. Intravenous infusion of NE (0.5 nmol/…

Malemedicine.medical_specialtyEndotheliumMyogenic contractionBlood PressureNitric OxideConstrictionNorepinephrineArterioleCricetinaeInternal medicinemedicine.arteryAbdomenInternal MedicinemedicineAnimalsVasoconstrictor AgentsMesocricetusChemistryAngiotensin IIAnatomyAngiotensin IIArteriolesmedicine.anatomical_structureEndocrinologycardiovascular systemVascular resistanceEndothelium VascularNitric Oxide Synthasemedicine.symptomVasoconstrictionBlood vesselHypertension
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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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Capillary flow and diameter changes during reperfusion after global cerebral ischemia studied by intravital video microscopy.

2004

The reaction of cerebral capillaries to ischemia is unclear. Based on Hossmann's observation of postischemic “delayed hypoperfusion,” we hypothesized that capillary flow is decreased during reperfusion because of increased precapillary flow resistance. To test this hypothesis, we measured cerebral capillary erythrocyte velocity and diameter changes by intravital microscopy in gerbils. A cranial window was prepared over the frontoparietal cortex in 26 gerbils anesthetized with halothane. The animals underwent either a sham operation or fifteen minutes of bilateral carotid artery occlusion causing global cerebral ischemia. Capillary flow velocities were measured by frame-to-frame tracking of…

Malemedicine.medical_specialtyPathologyIschemia030218 nuclear medicine & medical imagingBrain IschemiaBrain ischemia03 medical and health sciences0302 clinical medicineArteriolemedicine.arteryInternal medicinemedicineLaser-Doppler FlowmetryAnimalsCerebral CortexMicroscopy Videobusiness.industryLaser Doppler velocimetrymedicine.diseaseCapillariesDisease Models AnimalNeurologyCerebrovascular CirculationReperfusion InjuryCardiologyNeurology (clinical)HalothaneCardiology and Cardiovascular MedicinebusinessGerbillinaeReperfusion injuryPerfusion030217 neurology & neurosurgeryIntravital microscopymedicine.drugJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
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Betulinic Acid Protects from Ischemia-Reperfusion Injury in the Mouse Retina

2021

Ischemia/reperfusion (I/R) events are involved in the pathophysiology of numerous ocular diseases. The purpose of this study was to test the hypothesis that betulinic acid protects from I/R injury in the mouse retina. Ocular ischemia was induced in mice by increasing intraocular pressure (IOP) to 110 mm Hg for 45 min, while the fellow eye served as a control. One group of mice received betulinic acid (50 mg/kg/day p.o. once daily) and the other group received the vehicle solution only. Eight days after the I/R event, the animals were killed and the retinal wholemounts and optic nerve cross-sections were prepared and stained with cresyl blue or toluidine blue, respectively, to count cells in…

Malemedicine.medical_specialtyretinagenetic structuresQH301-705.5ischemia-reperfusion injuryarteriolesVideo microscopyProtective AgentsArticlechemistry.chemical_compoundMicebetulinic acidInternal medicineBetulinic acidmedicineAnimalsBiology (General)AxonGanglion cell layerreactive oxygen speciesRetinaAnti-Inflammatory Agents Non-SteroidalRetinalGeneral Medicinemedicine.diseaseeye diseasesMice Inbred C57BLmedicine.anatomical_structureEndocrinologychemistryReperfusion InjuryOptic nervesense organsPentacyclic TriterpenesReperfusion injuryCells
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Short-Time Ocular Ischemia Induces Vascular Endothelial Dysfunction and Ganglion Cell Loss in the Pig Retina

2019

Visual impairment and blindness are often caused by retinal ischemia-reperfusion (I/R) injury. We aimed to characterize a new model of I/R in pigs, in which the intraocular pathways were not manipulated by invasive methods on the ocular system. After 12 min of ischemia followed by 20 h of reperfusion, reactivity of retinal arterioles was measured in vitro by video microscopy. Dihydroethidium (DHE) staining, qPCR, immunohistochemistry, quantification of neurons in the retinal ganglion cell layer, and histological examination was performed. Retinal arterioles of I/R-treated pigs displayed marked attenuation in response to the endothelium-dependent vasodilator, bradykinin, compared to sham-tre…

Retinal Ganglion CellsVascular Endothelial Growth Factor A0301 basic medicinePathologySwineNitric Oxide Synthase Type IIVasodilationendothelial dysfunctionlcsh:Chemistrychemistry.chemical_compound0302 clinical medicineIschemiaEndothelial dysfunctionlcsh:QH301-705.5SpectroscopyGeneral MedicineComputer Science ApplicationsArteriolesmedicine.anatomical_structureRetinal ganglion cellReperfusion InjuryNADPH Oxidase 2medicine.medical_specialtyEndotheliumRetinal ArteryI/R injuryIschemiaretinal arteriolesBradykininRetinal ganglionRetinaArticleCatalysisganglion cell lossInorganic Chemistry03 medical and health sciencesmedicineAnimalsPhysical and Theoretical ChemistryMolecular BiologyRetinabusiness.industryOrganic ChemistryRetinalHypoxia-Inducible Factor 1 alpha Subunitmedicine.disease030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistry030221 ophthalmology & optometryEndothelium VascularReactive Oxygen SpeciesbusinessInternational Journal of Molecular Sciences
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