Search results for "S-Nitroso-N-acetylpenicillamine"

showing 5 items of 5 documents

Synthesis of nitric oxide in the dorsal motor nucleus of the vagus mediates the inhibition of gastric acid secretion by central bombesin

1999

1. Central administration of bombesin inhibits gastric acid production independently of the centrally or peripherally-acting stimuli employed. This study evaluates the role and location of the cerebral nitric oxide (NO) implicated in the inhibitory effect of central bombesin on in vivo rat gastric acid secretion, as induced by distension with 15 cm H2O, insulin (0.75 u.i. kg-1 i.p.) TRH (1.2 microg kg-1, i.c.) or pentagastrin (100 microg kg-1, i.p.). 2. The acid-inhibitory effect of i.c. bombesin (40 ng kg-1) was prevented by prior administration of L-NAME (80 microg kg-1) in the dorsal motor nucleus of the vagus (DMN). This dose of L-NAME when administered into the nucleus of the tractus s…

Pharmacologymedicine.medical_specialtySolitary nucleusBombesinThyrotropin-releasing hormoneBiologyPentagastrinchemistry.chemical_compoundEndocrinologyDorsal motor nucleuschemistryHypothalamusInternal medicinemedicineGastric acidS-Nitroso-N-acetylpenicillaminehuman activitieshormones hormone substitutes and hormone antagonistsmedicine.drugBritish Journal of Pharmacology
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Nitric oxide-mediated beta 2-adrenoceptor relaxation is impaired in mesenteric veins from portal-hypertensive rats.

1996

Abstract BACKGROUND & AIMS: beta-Adrenergic relaxation seems to be mediated by nitric oxide. The aim of this study was to evaluate changes induced by portal hypertension in beta 2-adrenergic vasorelaxation. METHODS: Isolated rat mesenteric veins were relaxed by salbutamol, and nerve- mediated vasocontractions were induced by electrical field stimulation. Responses were evaluated in the presence of NG-nitro-L-arginine methyl ester (L-NAME) or tetrodotoxin. Immunocytochemical techniques were used for localization of neuronal NO synthase. RESULTS: Salbutamol-induced relaxations were decreased in rings from portal-hypertensive animals. L- NAME reduced these relaxations, but its effects were mor…

Malemedicine.medical_specialtyVasodilator AgentsStimulationVasodilationTetrodotoxinIn Vitro TechniquesS-Nitroso-N-AcetylpenicillamineNitric OxideNitric oxideRats Sprague-Dawleychemistry.chemical_compoundMesenteric VeinsInternal medicinePapaverineHypertension PortalReceptors Adrenergic betamedicineAnimalsAlbuterolHepatologybiologyPenicillamineGastroenterologyAdrenergic beta-AgonistsImmunohistochemistryElectric StimulationRatsNitric oxide synthaseVasodilationEndocrinologymedicine.anatomical_structureNG-Nitroarginine Methyl EsterchemistryTetrodotoxinbiology.proteinS-Nitroso-N-acetylpenicillamineNitric Oxide SynthaseFree nerve endingBlood vesselGastroenterology
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Nitric oxide inhibits electrically active units in the rat pineal gland.

1997

Extracellular multiple unit recordings were performed in isolated rat pineal glands to determine a possible effect of nitric oxide (NO) on the spontaneous electrical activity of pinealocytes. Spontaneously active cells forming clusters of 3-5 cells fell into two categories: more or less regularly firing clusters (REG, 64%) and irregularly discharging clusters with periodically repeated bursts (RHY, 36%). The NO-donor sodium nitroprusside (SNP) reduced the discharge rate of the great majority of REG clusters and of all the RHY clusters examined. Moreover, the burst activity of RHY clusters was abolished. These results could be completely reproduced by using another NO-donor, S-nitroso-N-acet…

MaleNitroprussidemedicine.medical_specialtyTime FactorsIn Vitro TechniquesS-Nitroso-N-AcetylpenicillamineNitric OxidePineal GlandNitric oxidePinealocyteMembrane PotentialsRats Sprague-Dawleychemistry.chemical_compoundPineal glandInternal medicineExtracellularmedicineAnimalsBiological PsychiatryPenicillamineSnapNeural InhibitionRatsElectrophysiologyPsychiatry and Mental healthElectrophysiologyEndocrinologymedicine.anatomical_structureNeurologychemistryBiophysicsNeurology (clinical)Sodium nitroprussideEndocrine glandmedicine.drugSignal TransductionJournal of neural transmission (Vienna, Austria : 1996)
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Differential effects of nitric oxide donors on basal and electrically evoked release of acetylcholine from guinea-pig myenteric neurones

1996

1. The effects of the nitric oxide (NO) donors, 3-morpholino-sydnonimine (SIN-1), S-nitroso-N-acetylpenicillamine (SNAP) and sodium nitroprusside on basal and electrically evoked release of [3H]-acetylcholine were studied in myenteric plexus longitudinal muscle preparations of the guinea-pig small intestine preincubated with [3H]-choline. 2. The NO donors concentration-dependently increased basal release of [3H]-acetylcholine. The increase in release was calcium-dependent and was prevented in the presence of tetrodotoxin. Superoxide dismutase (150 u ml-1) potentiated the effect of SIN-1. The selective inhibitor of soluble guanylyl cyclase, 1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one (OD…

Malemedicine.medical_specialtyGuinea PigsMyenteric PlexusNitric Oxidechemistry.chemical_compoundInternal medicinemedicineAnimalsEnzyme InhibitorsPhosphodiesterase inhibitorMyenteric plexusPharmacologyDose-Response Relationship DrugEndothelium-derived relaxing factorAcetylcholineElectric StimulationEndocrinologychemistryMolsidomineFemaleSodium nitroprussideS-Nitroso-N-acetylpenicillamineSoluble guanylyl cyclaseZaprinastAcetylcholineResearch Articlemedicine.drugBritish Journal of Pharmacology
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Inducible NO synthase confers chemoresistance in head and neck cancer by modulating survivin

2009

The dual role of the inducible NO synthase (iNOS) and NO signaling in head and neck squamous cell carcinoma (HNSCC) is a complex and can both promote or inhibit tumor progression. However, the underlying molecular mechanisms are not yet resolved in detail. We show for the first time that conditions, favoring low NO levels conferred resistance against cisplatin/taxol-induced apoptosis in HNSCC cell lines. Cytoprotection was mediated by survivin, because we observed its upregulation subsequent to low doses of the NO donors S-nitroso-N-acetyl-penicillamine (SNAP) and sodium nitroprusside (SNP) or ectopic expression of physiologic amounts of iNOS. Also, RNAi-mediated depletion of survivin block…

MaleUmbilical VeinsCancer ResearchSurvivinFluorescent Antibody TechniqueNitric Oxide Synthase Type IIApoptosisp38 Mitogen-Activated Protein KinasesInhibitor of Apoptosis ProteinsImmunoenzyme TechniquesPhosphatidylinositol 3-Kinaseschemistry.chemical_compoundLY294002Enzyme InhibitorsRNA Small InterferingAged 80 and overReverse Transcriptase Polymerase Chain ReactionCell CycleMiddle AgedCell cycleOncologyHead and Neck NeoplasmsCarcinoma Squamous CellFemaleMicrotubule-Associated ProteinsNitroprussidePaclitaxelImmunoblottingAntineoplastic AgentsS-Nitroso-N-AcetylpenicillamineBiologyCell LineDownregulation and upregulationSurvivinmedicineHumansNitric Oxide DonorsRNA MessengerneoplasmsProtein kinase BNitritesPI3K/AKT/mTOR pathwayAgedmedicine.diseaseAntineoplastic Agents PhytogenicHead and neck squamous-cell carcinomachemistryDrug Resistance NeoplasmTumor progressionImmunologyCancer researchEndothelium VascularCisplatinProto-Oncogene Proteins c-aktInternational Journal of Cancer
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