Search results for "toxin"

showing 10 items of 1434 documents

Differential effects of calcium channel antagonists (omega-conotoxin GVIA, nifedipine, verapamil) on the electrically-evoked release of [3H]acetylcho…

1990

Electrically-evoked release of [3H]acetylcholine from autonomic neurons (myenteric plexus), motoneurons (phrenic nerve) and the central nervous system (neocortex) was investigated in the presence and absence of the calcium channel antagonists omega-conotoxin GVIA, nifedipine and verapamil, whereby the same species (rat) was used in all experiments. Release of [3H]acetylcholine was measured after incubation of the tissue with [3H]choline. omega-Conotoxin GVIA markedly reduced (70%) the evoked release of [3H]acetylcholine from the myenteric plexus of the small intestine (IC50: 0.7 nmol/l) with a similar potency at 3 and 10 Hz stimulation. An increase in the extracellular calcium concentration…

Malemedicine.medical_specialtyNifedipinechemistry.chemical_elementMollusk VenomsMyenteric PlexusCalciumAutonomic Nervous Systemcomplex mixturesNifedipineomega-Conotoxin GVIAInternal medicinemedicineAnimalsMyenteric plexusPhrenic nervePharmacologyCerebral CortexMotor NeuronsVoltage-dependent calcium channelCalcium channelRats Inbred StrainsGeneral MedicineCalcium Channel BlockersAcetylcholineElectric StimulationRatsPhrenic NerveEndocrinologynervous systemchemistryVerapamilAnesthesiaVerapamilFemaleAcetylcholinemedicine.drugNaunyn-Schmiedeberg's archives of pharmacology
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GABAergic inhibition of nitric oxide-mediated relaxation of guinea-pig ileum

1999

The effects of GABA receptor agonists were investigated on guinea-pig isolated ileum longitudinal muscle with intact myenteric plexus. Electrical field stimulation (1 Hz, 10 s) of the histamine (1 microM)-precontracted preparation caused a contraction followed by a relaxation. Relaxations were inhibited by L-N(G)-nitroarginine (L-NA; EC50 3 microM) in a concentration-dependent manner. The inhibitory action of 10 microM L-NA was blocked by 10 microM L-arginine but not by D-arginine, which indicates that the relaxation was largely mediated by endogenous nitric oxide (NO). Tetrodotoxin (1 microM) reduced the relaxation only by about 50%. GABA and the GABA(B) agonist, baclofen, inhibited the fi…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIMuscle RelaxationGuinea PigsTetrodotoxinIn Vitro TechniquesGABAB receptorBicucullineNitric OxideNitroargininechemistry.chemical_compoundGABA receptorIleumInternal medicinemedicineAnimalsGABA-A Receptor AgonistsEnzyme InhibitorsGABA Agonistsgamma-Aminobutyric AcidMyenteric plexusPharmacologyMuscimolGABAA receptorMuscle SmoothGeneral MedicineBicucullineElectric StimulationBaclofenEndocrinologynervous systemchemistryMuscimolGABA-B Receptor AgonistsSaclofenBiophysicsFemaleNitric Oxide SynthaseHistaminemedicine.drugNaunyn-Schmiedeberg's Archives of Pharmacology
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Effects of nitroglycerin or pentaerithrityl tetranitrate treatment on the gene expression in rat hearts: evidence for cardiotoxic and cardioprotectiv…

2009

Nitroglycerin (NTG) and pentaerithrityl tetranitrate (PETN) are organic nitrates used in the treatment of angina pectoris, myocardial infarction, and congestive heart failure. Recent data show marked differences in the effects of NTG and PETN on the generation of reactive oxygen species. These differences are attributed to different effects of NTG and PETN on the expression of antioxidative proteins like the heme oxygenase-I. To analyze the expressional effects of NTG and PETN in a more comprehensive manner we performed whole genome expression profiling experiments using cardiac total RNA from NTG- or PETN-treated rats and DNA microarrays containing oligonucleotides representing 27,044 rat…

Malemedicine.medical_specialtyPentaerithrityl tetranitrateCardiotonic Agentsgenetic structuresPhysiologyBiologyCardiotoxinsAnginaNitroglycerinInternal medicineGene expressionGeneticsmedicineAnimalsPentaerythritol TetranitrateMyocardial infarctionRats WistarNitroglycerinDNA PrimersOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingMyocardiummedicine.diseaseMolecular biologyeye diseasesOrganic nitratesRatsGene Expression RegulationHeart failureCardiologysense organsmedicine.drugPhysiological genomics
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Evaluation by reverse phase HPLC of [3H]acetylcholine release evoked from the myenteric plexus of the rat.

1990

Myenteric plexus-longitudinal muscle strips isolated from the small intestine of rats were incubated with [3H]choline to measure the synthesis and the release of [3H]acetylcholine. To separate different radioactive compounds (acetylcholine, choline, phosphorylcholine) from both the tissue and the overflow a new method, the reverse phase HPLC, was used. The radiochromatogram following the injection of a [3H]choline-standard and a [14C]acetylcholine-standard onto the HPLC showed a clear separation of both isotopes with a recovery rate of roughly 100%. Incubation of the muscle strips with [3H]choline caused the synthesis of [3H]acetylcholine (30,000 dpm/preparation) that increased 2-fold, when…

Malemedicine.medical_specialtyPhosphorylcholineGuinea PigsScopolaminechemistry.chemical_elementMyenteric PlexusTetrodotoxinCalciumIn Vitro TechniquesCholinechemistry.chemical_compoundInternal medicineMuscarinic acetylcholine receptormedicineExtracellularOxotremorineCholineAnimalsMyenteric plexusChromatography High Pressure LiquidPharmacologyChromatographyOxotremorineGeneral MedicineReceptors MuscarinicAcetylcholineElectric StimulationRatsEndocrinologychemistryTetrodotoxinFemaleAcetylcholinemedicine.drugNaunyn-Schmiedeberg's archives of pharmacology
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Inhibition of mechanical activity by neurotensin in rat proximal colon: involvement of nitric oxide.

1997

The aim of the present study was to define the nature of inhibitory action of neurotensin in rat proximal colon. Mechanical activity was detected as changes of intraluminal pressure. Neurotensin (10(-10) to 10(-7) M), in the presence of atropine (10(-6) M), guanethidine (10(-6) M), and nifedipine (10(-8) M), induced a tetrodotoxin-insensitive inhibitory effect characterized by the complete disappearance of the spontaneous phasic contractions. The inhibitory effect of neurotensin (10(-7) M) was abolished by scorpion venom (Leiurus quinquestriatus hebraeus) (10(-6) g/ml) or high K+ (40 mM KCl), whereas it persisted in the presence of omega-conotoxin GVIA, (10(-7) M). N omega-nitro-L-arginine…

Malemedicine.medical_specialtyPhysiologyColonNeuropeptideScorpion VenomsTetrodotoxinIn Vitro TechniquesInhibitory postsynaptic potentialNitric Oxidecomplex mixturesNitric oxidechemistry.chemical_compoundomega-Conotoxin GVIAPhysiology (medical)Internal medicinemedicineAnimalsOmega-Conotoxin GVIAEnzyme InhibitorsRats WistarGuanethidineNeurotensinHepatologybiologyGastroenterologyRatsNitric oxide synthaseEndocrinologyNG-Nitroarginine Methyl EsterMechanism of actionchemistrybiology.proteinPotassiumFemalemedicine.symptomGastrointestinal MotilityPeptidesmedicine.drugNeurotensinThe American journal of physiology
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Neuronostatin: peripheral site of action in mouse stomach.

2015

Neuronostatin is a 13-amino acid peptide encoded by somatostatin gene. It is distributed in different organs including gastrointestinal tract and has been involved in the control of food intake and gastroin-testinal motility, likely through an action in the brain. So far, there are no reports about the occurrence of peripheral action sites in the gut. Therefore, the purpose of the present study was to examine, in the mouse, the effects of peripheral administration of neuronostatin on food intake within 24 h and on gastrointestinal motility and to analyse neuronostatin actions on the gastric and intestinal mechanical activity in isolated preparations in vitro. When compared with PBS-treated …

Malemedicine.medical_specialtyPhysiologyPeptide HormonesGastric motilityMotilityBiologyBiochemistrySettore BIO/09 - FisiologiaCellular and Molecular Neurosciencechemistry.chemical_compoundEatingMiceEndocrinologyInternal medicinemedicineAnimalsGastrointestinal tractGastric emptyingStomachdigestive oral and skin physiologyStomachIntestinesmedicine.anatomical_structureEndocrinologyNeuronostatin Food intake Gastric emptying Intestinal transitchemistryTetrodotoxinDuodenumCholinergicGastrointestinal MotilityPeptides
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Glucagon-like peptide-2 relaxes mouse stomach through vasoactive intestinal peptide release.

2009

Glucagon-like peptide-2 (GLP-2) influences different aspects of the gastrointestinal function, including epithelial growth, digestion, absorption, motility, and blood flow. Intraluminal pressure from isolated mouse stomach was recorded to investigate whether GLP-2 affects gastric tone and to analyze its mechanism of action. Regional differences between diverse parts of the stomach were also examined using circular muscular strips from fundus and antrum. In the whole stomach, GLP-2 (0.3–100 nM) produced concentration-dependent relaxation with a maximum that was about 75% of relaxation to 1 μM isoproterenol (IC50 = 2.5 nM). This effect was virtually abolished by desensitization of GLP-2 rece…

Malemedicine.medical_specialtyPhysiologyVasoactive intestinal peptideGastric motilityMotilityTetrodotoxinIn Vitro TechniquesPeptide hormoneBiologySettore BIO/09 - FisiologiaMiceenteric nervous systemPhysiology (medical)Internal medicineGlucagon-Like Peptide 2Pyloric AntrummedicineAnimalsChymotrypsingastric motilityGastric FundusEnzyme InhibitorsSympathomimeticsHepatologyStomachdigestive oral and skin physiologyIsoproterenolGastroenterologygastrointestinal hormoneGlucagon-like peptide-2Mice Inbred C57BLVIPNG-Nitroarginine Methyl EsterEndocrinologymedicine.anatomical_structureGastric EmptyingGastrointestinal hormoneGastrointestinal functionhormones hormone substitutes and hormone antagonistsSodium Channel BlockersVasoactive Intestinal Peptide
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Depolarization-induced influx of sodium in response to phenylephrine in rat atrial heart muscle.

1991

1. The effects of alpha 1-adrenoceptor stimulation on transmembrane potential, currents and ion fluxes were investigated in multicellular preparations and/or single cells obtained from the left atrium of rat hearts. 2. In multicellular preparations, phenylephrine caused a concentration-dependent positive inotropic effect, an increase in action potential duration, and a decrease in resting potential; the effects were antagonized by phentolamine. 3. In the presence of phenylephrine (100 mumol/1), two levels of resting potential were observed when the preparations were, alternately, electrically stimulated or kept at rest (-74 +/- 1 mV during activity and -62 +/- 4 mV at rest; mean +/- S.E.M.;…

Malemedicine.medical_specialtyPhysiologyVoltage clampAction PotentialsStimulationMembrane PotentialsPhenylephrinechemistry.chemical_compoundPhentolamineInternal medicinemedicineAnimalsHeart AtriaPhenylephrineMembrane potentialChemistryMyocardiumSodiumRats Inbred StrainsDepolarizationMyocardial ContractionResting potentialStimulation ChemicalRatsElectrophysiologyEndocrinologyTetrodotoxinCalciumResearch Articlemedicine.drugThe Journal of Physiology
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The effect of physostigmine on the vagally induced muscarinic inhibition of noradrenaline release from the isolated perfused rabbit atria.

1982

1. Presynaptic cholinergic-adrenergic interactions were studied on isolated perfused rabbit atria with the extrinsic right vagus and sympathetic innervation intact. The transmitter stores were labelled with 14C-choline and 3H-noradrenaline. The radioactive compounds were separated on columns and determined by scintillation spectrometry. The stimulation-evoked overflow of both transmitters was calcium-dependent and abolished by tetrodotoxin. 2. Methacholine caused a concentration-dependent decrease of atrial tension development and 3H-noradrenaline overflow evoked by 3 Hz sympathetic stimulation. Vagus nerve stimulation (1–20Hz), although nearly abolishing tension development at 20Hz, decrea…

Malemedicine.medical_specialtyPhysostigmineSympathetic Nervous Systemmedicine.medical_treatmentPhysostigmineIn Vitro TechniquesCholinechemistry.chemical_compoundNorepinephrineInternal medicineMuscarinic acetylcholine receptormedicineAnimalsCholinesterasesMethacholine CompoundsReceptors CholinergicAxonCholinesterasePharmacologybiologyChemistryMyocardiumVagus NerveGeneral MedicineReceptors MuscarinicElectric StimulationEndocrinologymedicine.anatomical_structurenervous systemcardiovascular systembiology.proteinTetrodotoxinMethacholineFemaleRabbitsVagus nerve stimulationAcetylcholinemedicine.drugNaunyn-Schmiedeberg's archives of pharmacology
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Acute ammonia intoxication induces an NMDA receptor-mediated increase in poly(ADP-ribose) polymerase level and NAD+ metabolism in nuclei of rat brain…

2004

Acute ammonia toxicity is mediated by excessive activation of NMDA receptors. Activation of NMDA receptors leads to activation of poly(ADP-ribose) polymerase (PARP) which mediates NMDA excitotoxicity. PARP is activated following DNA damage and may lead to cell death via NAD+ and ATP depletion. The aim of the present work was to assess whether acute ammonia intoxication in vivo leads to increased PARP in brain cells nuclei and to altered NAD+ and superoxide metabolism and the contribution of NMDA receptors to these alterations. Acute ammonia intoxication increases PARP content twofold in brain cells nuclei.NAD+ content decreased by 55% in rats injected with ammonia. This was not due to decre…

Malemedicine.medical_specialtyPoly ADP ribose polymeraseExcitotoxicityBiologymedicine.disease_causeReceptors N-Methyl-D-AspartateBiochemistryCellular and Molecular Neurosciencechemistry.chemical_compoundNAD+ NucleosidaseAmide SynthasesAmmoniaSuperoxidesInternal medicinemedicineAnimalsNeurotoxinRats WistarReceptorBrain ChemistryCell NucleusProtein Synthesis InhibitorsSuperoxideNAD+ ADP-RibosyltransferaseBrainProteinsNADMolecular biologyRatsEndocrinologychemistryTyrosineNMDA receptorNAD+ kinasePoly(ADP-ribose) PolymerasesJournal of Neurochemistry
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