Search results for "Rini"

showing 10 items of 746 documents

Muscarinic inhibition of [3H]-noradrenaline release on rabbit iris in vitro: effects of stimulation conditions on intrinsic activity of methacholine …

1988

1. Rabbit isolated irides were loaded with [3H]-noradrenaline and superfused with Tyrode solution. The inhibition by the muscarinic agonists (+/-)-methacholine and pilocarpine of the [3H]-noradrenaline overflow into the superfusate evoked by field stimulation (pulses of 1 ms duration, 75 mA) was measured as an index of activation of presynaptic muscarinic receptors. 2. The fractional rate of release per pulse during the first stimulation period (S1) was low with 360 pulses at 3 Hz, intermediate with 360 pulses at 10 Hz and high with 1200 pulses at 10 Hz. Upon repetitive stimulation (7 periods at 20 min intervals), the fractional rates of release per pulse during S7 no longer differed, sugge…

AtropineMalemedicine.medical_specialtyIrisStimulationIn Vitro TechniquesNorepinephrineInternal medicineMuscarinic acetylcholine receptormedicineAnimalsMethacholine CompoundsMethacholine ChlorideMethacholine CompoundsPharmacologyChemistryPilocarpineReceptors MuscarinicElectric StimulationAtropineIris dilator muscleEndocrinologyPilocarpineFemaleMethacholineRabbitsAcetylcholineResearch Articlemedicine.drugBritish Journal of Pharmacology
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Muscarinic inhibition of potassium-induced noradrenaline release and its dependence on the calcium concentration.

1975

1. Noradrenaline release from the isolated rabbit heart was evoked by perfusion with a medium containing 135 mM potassium and 17 mM sodium ions (high K+-low Na+). 2. The noradrenaline output in response to high K+-low Na+ was dose-dependently decreased by methacholine (0.625-320 muM) and this effect was reserved by atropine 1.44 mM. 3. Lowering the calcium concentration of high K+-low Na+ from 1.8-0.1125 mM decreased the noradrenaline output by 85%. The effect of methacholine, expressed as % inhibition of noradrenaline release, was potentiated by lowering of the calcium concentration. 4. Both at normal and lowered calcium concentrations the inhibitory action of methacholine was larger from …

AtropineMalemedicine.medical_specialtyReserpineTime FactorsSodiumPotassiumchemistry.chemical_elementAdrenergicCalciumchemistry.chemical_compoundNorepinephrineInternal medicineMuscarinic acetylcholine receptormedicinePressureAnimalsMethacholine CompoundsReceptors CholinergicPharmacologyCalcium metabolismMuscarineChemistryMyocardiumOsmolar ConcentrationSodiumGeneral MedicinePerfusionEndocrinologyPotassiumMethacholineCalciumFemaleRabbitsmedicine.drugNaunyn-Schmiedeberg's archives of pharmacology
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Effects of several muscarinic agonists on cardiac performance and the release of noradrenaline from sympathetic nerves of the perfused rabbit heart

1972

Summary 1 The effects of several muscarinic agonists on atrial tension development, ventricular rate and noradrenaline release from terminal sympathetic fibres evoked by electrical nerve stimulation (SNS) and 1,1-dimethyl-4-phenylpiperazinium (DMPP) were measured in isolated perfused rabbit hearts. 2 Hexamethonium, in a concentration which almost abolished the release of noradrenaline by DMPP, had no effect on the release produced by SNS, confirming that the stimulation was postganglionic. 3 The order of potency for inhibition of atrial tension development was N-methyl-1,2,5,6, tetrahydro-nicotinic acid prop-2-yne ester (MH-1)>oxotremorine > acetylcholine > methacholine > carbachol > furtre…

AtropineMalemedicine.medical_specialtySympathetic Nervous SystemCarbacholAutopharmacologyHexamethonium CompoundsIn Vitro TechniquesPharmacologyNorepinephrinechemistry.chemical_compoundHeart RateInternal medicineMuscarinic acetylcholine receptormedicineOxotremorineAnimalsMethacholine CompoundsPharmacologyChemistryOxotremorinePilocarpineHeartAcetylcholineElectric StimulationPerfusionQuaternary Ammonium CompoundsAtropineEndocrinologyParasympathomimeticsPilocarpineCarbacholFemaleMethacholineHexamethoniumCarbamatesRabbitsDimethylphenylpiperazinium IodideAcetylcholinemedicine.drugBritish Journal of Pharmacology
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Short- and long-latency muscarinic inhibition of noradrenaline release from rabbit atria induced by vagal stimulation.

1988

1. The influence of the time interval between vagal and sympathetic nerve stimuli on the magnitude of muscarinic inhibition of noradrenaline release was studied in the isolated perfused rabbit atria preparation. The transmitter stores were labelled with [14C]choline and [3H]noradrenaline. 2. The right cardiac postganglionic sympathetic nerves were stimulated at 3 Hz for 3 min three times at intervals of 10 min. The [3H]noradrenaline outflow evoked by the second stimulation equalled the averaged means of the log values of amine outflows evoked by the first and third stimulations. 3. During the second sympathetic stimulation the right vagus nerve was stimulated (3 Hz, 3 min) in such a way tha…

AtropineMalemedicine.medical_specialtySympathetic Nervous SystemTime FactorsPhysiologyAdrenergicTubocurarineStimulationIn Vitro TechniquesInhibitory postsynaptic potentialCholineNorepinephrineInternal medicineMuscarinic acetylcholine receptormedicineAnimalsChemistryMyocardiumVagus NerveReceptors MuscarinicAcetylcholineAtropineEndocrinologyCholinergicSilent periodFemaleRabbitsAcetylcholinemedicine.drugResearch Article
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A muscarinic inhibition of the noradrenaline release evoked by postganglionic sympathetic nerve stimulation

1969

1. The noradrenaline output from isolated rabbit hearts perfused with Tyrode solution was estimated fluorimetrically. The postganglionic sympathetic nerves of the heart were stimulated (10 shocks/sec; 1 msec) for three 1 min periods with intervals of 10 min. 2. The noradrenaline output evoked by 3 consecutive stimulation periods decreased exponentially. 3. Acetylcholine (10−9–10−6 g/ml) administered continuously one min before to one min after the second stimulation caused a dose-dependent reduction of the noradrenaline output evoked by the second stimulation to as low as 19% of the normal value. Acetylcholine in the concentrations applied did not cause a noradrenaline output by itself. 4. …

AtropineMalemedicine.medical_specialtySympathetic Nervous SystemTyramineStimulationHexamethonium CompoundsIn Vitro TechniquesPiperazinesNorepinephrinechemistry.chemical_compoundInternal medicineMuscarinic acetylcholine receptormedicineAnimalsMethacholine CompoundsFluorometryReceptors CholinergicPharmacologyHeartAdrenergic nervous systemGeneral MedicineCoronary VesselsAcetylcholineElectric StimulationReceptors AdrenergicPerfusionQuaternary Ammonium CompoundsAtropineEndocrinologyParasympathomimeticschemistryDepression ChemicalAutonomic Fibers PostganglionicCholinergicFemaleHexamethoniumMethacholineRabbitsAcetylcholinemedicine.drugNaunyn-Schmiedebergs Archiv f�r Pharmakologie
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Primary peristalsis in pigeon cervical oesophagus: two EMG patterns.

1984

Swallowing elicits two propagated EMG peristaltic patterns in pigeon cervical oesophagus: i) "simple" peristaltic pattern and ii) "complex" peristaltic pattern. "Simple" peristaltic pattern is characterized by an intense, long-lasting burst of spikes, high in amplitude with an aboral increasing delay in onset. "Complex" peristaltic pattern presents an early short period of reduction in spontaneous electrical activity, followed by an excitatory period similar to that of "simple" pattern. The early inhibitory component has a very short delay in onset increasing aborally. Atropine abolishes the EMG excitatory component of both patterns, while the inhibitory period persists, showing increased d…

AtropinePhysiologyElectromyographyCholinergic NervesAnatomyBiologyInhibitory postsynaptic potentialBiochemistryElectrophysiologyCervical oesophagusEsophagusMuscarinic acetylcholine receptorExcitatory postsynaptic potentialCholinergicAnimalsPeristalsisColumbidaeGastrointestinal MotilityPeristalsisArchives internationales de physiologie et de biochimie
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Cholinesterase activity and exposure time to acetylcholine as factors influencing the muscarinic inhibition of [3H]-noradrenaline overflow from guine…

1985

Guinea-pig isolated atria were incubated and loaded with [3H]-noradrenaline. The release of 3H and of [3H]-noradrenaline was induced by field stimulation (6-9 trains of 150 pulses at 5 Hz). The stimulation-evoked overflows of 3H and of [3H]-noradrenaline were determined. In the absence of an inhibitor of acetylcholinesterase, acetylcholine (12 min preincubation before nerve stimulation, up to 10 microM) failed to inhibit the evoked [3H]-noradrenaline overflow. In the presence of atropine, an increase by acetylcholine of evoked release was observed in the same atria. In contrast, the selective muscarinic agonist methacholine significantly decreased the evoked overflow. The inhibition was ant…

AtropinePhysostigminemedicine.medical_specialtyTime FactorsPhysostigmineGuinea PigsHexamethonium CompoundsIn Vitro TechniquesHexamethoniumMuscarinic agonistNorepinephrinechemistry.chemical_compoundCocaineInternal medicineMuscarinic acetylcholine receptormedicineAnimalsMethacholine CompoundsDrug InteractionsHeart AtriaPhentolamineMethacholine ChlorideCholinesterasePharmacologybiologyHeartPropranololReceptors MuscarinicAcetylcholineAtropineEndocrinologychemistryAcetylcholinesterasebiology.proteinMethacholineHexamethoniumCorticosteroneAcetylcholineResearch Articlemedicine.drugBritish Journal of Pharmacology
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Acetylcholine via Muscarinic Receptors Inhibits Histamine Release from Human Isolated Bronchi

1997

Human bronchi were incubated in organ baths to measure histamine release. The calcium ionophore A23187 (10 mumol/L; 1 min) stimulated histamine release by 148 +/- 28% (n = 11) above the prestimulation level but was ineffective in epithelium-denuded bronchi. Neither bradykinin (0.1 mumol/L) nor compound 48/80 (10 micrograms/ml) triggered the release of histamine from epithelium-intact bronchi. Acetylcholine did not affect spontaneous histamine release (about 2 nmol/g x 5 min) but inhibited A23187-evoked histamine release in an atropine-sensitive manner. Already a concentration as low as 0.1 nmol/L acetylcholine was effective, the maximal inhibition (by 89%) occurred at 100 nmol/L, whereas a …

AtropinePulmonary and Respiratory MedicineAgonistPhysostigminemedicine.medical_specialtyTime Factorsmedicine.drug_classPhysostigmineBradykininBronchiMuscarinic AntagonistsMuscarinic AgonistsCritical Care and Intensive Care MedicineHistamine Releasechemistry.chemical_compoundCulture TechniquesInternal medicineMuscarinic acetylcholine receptormedicineOxotremorineHumansDrug InteractionsCalcimycinDose-Response Relationship DrugIonophoresbusiness.industryOxotremorineImmunoglobulin EReceptors MuscarinicAcetylcholineEndocrinologychemistryAcetylcholinesterase inhibitorDepression ChemicalCholinesterase InhibitorsbusinessAcetylcholineHistaminemedicine.drugAmerican Journal of Respiratory and Critical Care Medicine
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Release of [3H]Acetylcholine in Human Isolated Bronchi: Effect of Indomethacin on Muscarinic Autoinhibition

1995

Receptor-mediated regulation of acetylcholine release in the airways, particularly in humans, remains unclear. In the present study, the tissue content of acetylcholine and release of [3H]acetylcholine were measured in freshly dissected human bronchi obtained at thoracotomy. Large (main and lobar bronchi) and small (segmental and subsegmental bronchi) airways contained considerable amounts of endogenous acetylcholine (300 +/- 50 pmol/100 mg wet weight), whereas significantly less was found in lung parenchyma (60 +/- 30 pmol/100 mg). Isolated small bronchi incubated in an organ bath with the precursor [3H]choline synthesized significant amounts of [3H]acetylcholine (26,000 +/- 4,000 dpm/100 …

AtropinePulmonary and Respiratory Medicinemedicine.medical_specialtyIndomethacinStimulationBronchiIn Vitro TechniquesCritical Care and Intensive Care Medicinechemistry.chemical_compoundInternal medicineMuscarinic acetylcholine receptormedicineOxotremorineCholineHumansbusiness.industryOxotremorinerespiratory systemReceptors MuscarinicAcetylcholineElectric StimulationAtropineEndocrinologychemistryTetrodotoxinCholinergicbusinessAcetylcholinemedicine.drugAmerican Journal of Respiratory and Critical Care Medicine
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Use of atropine-treated Daphnia magna survival for detection of environmental contamination by acetylcholinesterase inhibitors.

2003

The toxicity of cholinesterase-inhibiting compounds (e.g., carbamates and organophosphates) is due to a decrease in acetylcholine metabolism, which results in a continuous stimulation of cholinergic receptors (muscarinic and nicotinic) that can be fatal. The goal of this study was to evaluate the protective effect of atropine (muscarinic receptor antagonist) against paraoxon-induced toxicity to Daphnia magna using its survival rate for the detection of environmental contamination by cholinesterase-inhibiting compounds. As expected, paraoxon was lethal to D. magna in a concentration-dependent manner. Noteworthy, the pretreatment of these organisms with atropine dramatically increased their s…

AtropineSurvivalHealth Toxicology and MutagenesisDaphnia magnaMuscarinic AntagonistsBiologyPharmacologyParaoxonToxicologychemistry.chemical_compoundMuscarinic acetylcholine receptormedicineAnimalsreproductive and urinary physiologyParaoxonfungiPublic Health Environmental and Occupational HealthGeneral Medicinebiology.organism_classificationPollutionAcetylcholinesteraseAtropineNicotinic agonistchemistryDaphniaToxicityCholinergicCholinesterase InhibitorsBiomarkersWater Pollutants Chemicalmedicine.drugEcotoxicology and environmental safety
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