Search results for "Nitric Oxide Donor"

showing 9 items of 39 documents

NANC inhibitory neurotransmission in mouse isolated stomach: Involvement of nitric oxide, ATP and vasoactive intestinal polypeptide

2003

1. The neurotransmitters involved in NANC relaxation and their possible interactions were investigated in mouse isolated stomach, recording the motor responses as changes of endoluminal pressure from whole organ. 2. Field stimulation produced tetrodotoxin-sensitive, frequency-dependent, biphasic responses: rapid transient relaxation followed by a delayed inhibitory component. 3. The inhibitor of the synthesis of nitric oxide (NO), L-NAME, abolished the rapid relaxation and significantly reduced the slow relaxation. Apamin, blocker of Ca 2+-dependent K + channels, or ADPβS, which desensitises P 2y purinoceptors, reduced the slow relaxation to 2-8 Hz, without affecting that to 16-32 Hz or the…

NitroprussideMuscle RelaxationNANC inhibitory neurotransmitterNitric OxideSynaptic TransmissionSettore BIO/09 - FisiologiaGastric relaxationMiceAdenosine TriphosphateAdrenergic FiberChymotrypsinEnzyme InhibitorThionucleotideCholinergic FiberPharmacologyDose-Response Relationship DrugAnimalIn Vitro TechniqueMouse stomachStomachNitric Oxide DonorElectric StimulationATPVIPAdenosine DiphosphateMice Inbred C57BLNG-Nitroarginine Methyl EsterApaminReceptors Vasoactive Intestinal PeptideNitric Oxide SynthaseVasoactive Intestinal Peptide
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Involvement of PKC and NF-κB in Nitric Oxide Induced Apoptosis in Human Coronary Artery Smooth Muscle Cells

2001

Apoptosis of vascular smooth muscle cells is critically involved in progression of atherosclerosis and may prevent intimal hyperplasia in restenosis and vascular remodeling. Nitric oxide (NO) is known to induce apoptosis, but the signaling pathways still remain unclear. We investigated p53 accumulation, protein kinase C (PKC) activation and nuclear transcription factor (NF-kappaB) binding activity as possible signaling mechanisms of NO-induced apoptosis. Apoptosis was induced dose-dependently with the NO-donors sodiumnitroprusside (SNP: 232+/-48%) and SIN-1 (241+/-90% of actinomycin D induced apoptosis; means +/- SEM, *por =0.05 vs. control) in HSMC. Inhibition of PKC significantly attenuat…

Nitroprussidemedicine.medical_specialtyVascular smooth muscleIntimal hyperplasiaPhysiologyApoptosisDNA FragmentationNaphthalenesNitric OxideMuscle Smooth VascularNitric oxidechemistry.chemical_compoundNF-KappaB Inhibitor alphaRestenosisInternal medicinemedicineHumansNitric Oxide DonorsEnzyme InhibitorsCells CulturedProtein Kinase CProtein kinase CCell Nucleusbusiness.industryNF-kappa BNF-κBStaurosporinemedicine.diseaseCoronary VesselsDNA-Binding Proteinsmedicine.anatomical_structurechemistryApoptosisMolsidomineCancer researchCardiologyI-kappa B ProteinsTumor Suppressor Protein p53businessArteryCellular Physiology and Biochemistry
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Possible roles of nitric oxide in the physiology and pathophysiology of the guinea pig cochlea.

2000

Two nitric oxide synthase isoforms (NOS-I and NOS-III) are present in the mammalian cochlea, and many regulatory functions of the inner ear could be mediated by NO. In this study, cochlear potentials and immunohistochemical measures were analyzed by changing the concentration of NO in the guinea pig during intracochlear and intravenous application of an NOS inhibitor and an NO donor. In anesthetized guinea pigs the NOS inhibitor NG-nitro-L-arginine-methylester (L-NAME) was applied by intracochlear perfusion or intravenously. The cochlear potentials and blood pressure were measured during and after the application. Cochleae were removed and prepared for morphological and immunohistochemical …

Pathologymedicine.medical_specialtyGuinea PigsPhysiologyBiologyNitric oxideGuinea pigchemistry.chemical_compoundotorhinolaryngologic diseasesmedicineAnimalsInner earNitric Oxide DonorsOrgan of CortiCochleaPenicillamineSnapGeneral MedicineImmunohistochemistryGanglionCochleaNitric oxide synthasemedicine.anatomical_structureNG-Nitroarginine Methyl EsterOtorhinolaryngologychemistryInjections Intravenousbiology.proteinFemalesense organsNitric Oxide SynthasePerfusionEuropean archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
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Role of Nitric Oxide in Gastrointestinal Inflammatory and Ulcerative Diseases: Perspective for Drugs Development

2001

Nitric oxide is a ubiquitous molecule involved in a variety of biological processes. The specific action of NO depends on its enzymatic sources namely neuronal nitric oxide synthase (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS) and all three isoforms have been localized in the gastrointestinal tract. Constitutive synthesis of NO by nNOS or eNOS isoforms is involved in the maintaining of the gastrointestinal mucosal integrity through modulation of gastric mucosal blood flow, epithelial secretion and barrier function. However, large amounts of NO synthesized from the inducible isoform have been implicated in tissue injury in the gut during inflammatory reactions. In this review we p…

Peptic UlcerNitric Oxide Synthase Type IIPharmacologyNitric OxideEndothelial NOSNitric oxidechemistry.chemical_compoundGastrointestinal AgentsEnosDrug DiscoverymedicineAnimalsHumansNitric Oxide DonorsEnzyme InhibitorsBarrier functionPharmacologyGastrointestinal tractbiologyAnti-Ulcer Agentsbiology.organism_classificationEpitheliumGastroenteritisNitric oxide synthasemedicine.anatomical_structureMechanism of actionchemistryImmunologybiology.proteinNitric Oxide Synthasemedicine.symptomCurrent Pharmaceutical Design
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Role of nitric oxide synthase isoforms for ophthalmic artery reactivity in mice.

2014

Abstract Nitric oxide synthases (NOS) are involved in regulation of ocular vascular tone and blood flow. While endothelial NOS (eNOS) has recently been shown to mediate endothelium-dependent vasodilation in mouse retinal arterioles, the contribution of individual NOS isoforms to vascular responses is unknown in the retrobulbar vasculature. Moreover, it is unknown whether the lack of a single NOS isoform affects neuron survival in the retina. Thus, the goal of the present study was to examine the hypothesis that the lack of individual nitric oxide synthase (NOS) isoforms affects the reactivity of mouse ophthalmic arteries and neuron density in the retinal ganglion cell (RGC) layer. Mice defi…

Retinal Ganglion CellsVasodilator AgentsNitric Oxide Synthase Type IIVideo microscopyVasodilationCell CountNitric Oxide Synthase Type IMuscle Smooth Vascularchemistry.chemical_compoundMiceOphthalmic ArteryPhenylephrineEnosEnzyme InhibitorsMice KnockoutbiologyAnatomySensory SystemsNitric oxide synthaseIsoenzymesVasodilationmedicine.anatomical_structureNG-Nitroarginine Methyl EsterRetinal ganglion cellKnockout mouseRetinal NeuronsNitroprussidemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndothelial NOSNitric oxideCellular and Molecular NeuroscienceTonometry OcularInternal medicinemedicineAnimalsNitric Oxide DonorsIntraocular Pressurebusiness.industrybiology.organism_classificationAcetylcholineMice Inbred C57BLOphthalmologyEndocrinologychemistryVasoconstrictionbiology.proteinAdrenergic alpha-1 Receptor AgonistsEndothelium VascularbusinessExperimental eye research
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Nitric Oxide-Releasing Drug Glyceryl Trinitrate Targets JAK2/STAT3 Signaling, Migration and Invasion of Triple-Negative Breast Cancer Cells

2021

Triple-negative breast cancer (TNBC) is a highly aggressive disease with invasive and metastasizing properties associated with a poor prognosis. The STAT3 signaling pathway has shown a pivotal role in cancer cell migration, invasion, metastasis and drug resistance of TNBC cells. IL-6 is a main upstream activator of the JAK2/STAT3 pathway. In the present study we examined the impact of the NO-donor glyceryl trinitrate (GTN) on the activation of the JAK2/STAT3 signaling pathway and subsequent migration, invasion and metastasis ability of TNBC cells through in vitro and in vivo experiments. We used a subtoxic dose of carboplatin and/or recombinant IL-6 to activate the JAK2/STAT3 signaling path…

STAT3 Transcription FactorQH301-705.5Triple Negative Breast NeoplasmsmigrationArticleCatalysisStat3 Signaling PathwayMetastasisInorganic ChemistryMiceNitroglycerinchemistry.chemical_compoundCell Movementnitric oxideIn vivoCell Line TumormedicineAnimalsHumanscancermetastasisNeoplasm InvasivenessNitric Oxide DonorsBiology (General)Physical and Theoretical ChemistrySTAT3QD1-999Molecular BiologySpectroscopyTriple-negative breast cancerMice Inbred BALB CbiologyActivator (genetics)Organic ChemistryCancerGeneral MedicineJanus Kinase 2invasionmedicine.diseaseCarboplatinComputer Science ApplicationsChemistrychemistrybiology.proteinCancer researchFemalesignalingSignal TransductionInternational Journal of Molecular Sciences
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Nitric oxide increases the decay of matrix metalloproteinase 9 mRNA by inhibiting the expression of mRNA-stabilizing factor HuR.

2003

Dysregulation of extracellular matrix turnover is an important feature of many inflammatory processes. Rat renal mesangial cells express high levels of matrix metalloproteinase 9 (MMP-9) in response to inflammatory cytokines such as interleukin-1 beta. We demonstrate that NO does strongly destabilize MMP-9 mRNA, since different luciferase reporter gene constructs containing the MMP-9 3' untranslated region (UTR) displayed significant reduced luciferase activity in response to the presence of NO. Moreover, by use of an in vitro degradation assay we found that the cytoplasmic fractions of NO-treated cells contained a higher capacity to degrade MMP-9 transcripts than those obtained from contro…

Untranslated regionCytoplasmRNA StabilityMolecular Sequence DataGene ExpressionRNA-binding proteinBiologyKidneyNitric OxideELAV-Like Protein 1Gene expressionAnimalsElectrophoretic mobility shift assayNitric Oxide DonorsRNA MessengerEnzyme InhibitorsMolecular Biology3' Untranslated RegionsCyclic GMPCells CulturedRepetitive Sequences Nucleic AcidMessenger RNABase SequenceThree prime untranslated regionMolecular MimicryRNARNA-Binding ProteinsCell BiologyMolecular biologyRecombinant ProteinsRatsELAV ProteinsMatrix Metalloproteinase 9RibonucleoproteinsGuanylate CyclaseAntigens SurfaceAminoquinolinesDactinomycinSoluble guanylyl cyclaseInterleukin-1Nitroso CompoundsMolecular and cellular biology
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The phototransduction cascade in the isolated chick pineal gland revisited.

2003

It is well established that the isolated chick pineal gland is directly light sensitive and that melatonin synthesis of the gland can be inhibited by exposing the gland to light during scotophase. Since not all the steps of the phototransduction cascade have been clarified to the same extent as in the retina, we have treated isolated chick pineal glands with 90 min of light during scotophase and with drugs that affect key-components of vertebrate phototransduction, i.e., cyclic guanosine monophosphate (cGMP) phosphodiesterase 6 (PDE6), cGMP levels and cGMP-gated calcium channels. The endpoint measured was the activity of the rate-limiting enzyme of melatonin synthesis, arylalkylamine N-acet…

medicine.medical_specialtyLight Signal TransductionArylamine N-AcetyltransferasePhosphodiesterase 3BiologyNitric OxidePineal GlandRetinachemistry.chemical_compoundPineal glandOrgan Culture TechniquesInternal medicinemedicineCyclic AMPAnimalsCyclic adenosine monophosphateNitric Oxide DonorsEnzyme InhibitorsMolecular BiologyCyclic guanosine monophosphateCyclic GMPMelatoninCyclic Nucleotide Phosphodiesterases Type 6Phosphoric Diester HydrolasesGeneral NeurosciencePhosphodiesteraseNatriuretic Peptide C-TypeCyclic Nucleotide Phosphodiesterases Type 3Circadian RhythmCalcium Channel Agonistsmedicine.anatomical_structureEndocrinologychemistry3'5'-Cyclic-AMP PhosphodiesterasesNeurology (clinical)PDE10ACalcium ChannelsZaprinastChickensPhotic StimulationDevelopmental BiologyEndocrine glandBrain research
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An overview of new pharmacological treatments for cerebrovascular dysfunction after experimental subarachnoid hemorrhage

2004

Cerebral vasospasm and the resulting cerebral ischemia occurring after subarachnoid hemorrhage (SAH) are still responsible for the considerable morbidity and mortality in patients affected by cerebral aneurysms. Mechanisms contributing to the development of vasospasm, abnormal reactivity of cerebral arteries and cerebral ischemia after SAH have been intensively investigated in recent years. It has been suggested that the pathogenesis of vasospasm is related to a number of pathological processes, including endothelial damage, smooth muscle cell contraction resulting from spasmogenic substances generated during lyses of subarachnoid blood clots, changes in vascular responsiveness and inflamma…

medicine.medical_specialtyPotassium ChannelsSubarachnoid hemorrhageCerebral arteriesIschemiaNeuroprotectionCerebral vasospasmInternal medicinemedicineAnimalsHumansNitric Oxide Donorscardiovascular diseasesErythropoietinVascular diseasebusiness.industryEndothelinsGeneral NeuroscienceVasospasmSubarachnoid Hemorrhagemedicine.diseaseRecombinant Proteinsnervous system diseasesCerebrovascular DisordersErythropoietinAnesthesiaCardiologyNeurology (clinical)businessmedicine.drugBrain Research Reviews
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