Search results for "Agoni"

showing 10 items of 2493 documents

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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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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Muscarinic Modulation of Acetylcholine Release from the Myenteric Plexus of the Guinea Pig Small Intestine

1978

The concept of a local feedback regulation of neurotransmitter release has been most intensively studied in the adrenergic system (See Ref. 13 for review). The feedback hypothesis of noradrenaline release is based on the findings that α-adrenolytic drugs enhance, and α-adrenoceptor agonists reduce neuronal noradrenaline release. Relatively few systematic studies have been made on the influence of cholinolytic and cholinomimetic drugs on the release of ACh. Szerb and Somogyi (14) reported that the potent muscarinic agonist oxotremorine inhibited ACh output from cerebral cortical slices. Further, the muscarinic antagonists atropine and hyoscine have been found to facilitate the release of ACh…

Atropinechemistry.chemical_compoundchemistryMuscarinic acetylcholine receptormedicineOxotremorineAdrenergicPharmacologyNeurotransmitterMuscarinic agonistAcetylcholineMyenteric plexusmedicine.drug
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Mode and mechanism of neurotensin action in rat proximal colon

1997

Abstract This study examined the mechanism of action of neurotensin on intraluminal pressure in rat proximal colon. The direct and indirect contractile response to neurotensin (100 nM) was abolished in Ca 2+ -free solution, and was antagonized by nifedipine (1–5–10 nM) and potentiated by Bay K 8644 (methyl 1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-pyridine-5-carboxylate) (10–100–1000 nM). Neurotensin, in the presence of nifedipine (10 nM) and atropine (1 μM), induced a tetrodotoxin-insensitive inhibitory effect, which was antagonized by SR 48692 (2[(1-(7-chloro-4-quinolinyl)-5-(2,6-dimethoxy-phenyl)pyrazol-3-yl) carbonyl amino]tricyclo (3.3.1.1. 3.7 ) decan-2-carboxylic a…

Atropinemedicine.medical_specialtyNifedipineColonchemistry.chemical_elementCholinergic AgonistsIn Vitro TechniquesCalciumInhibitory postsynaptic potentialApaminCholinergic Antagonistschemistry.chemical_compoundNifedipineInternal medicinemedicineAnimalsReceptors NeurotensinRats WistarNeurotensinPharmacologyChemistryMuscle Smooth3-Pyridinecarboxylic acid 14-dihydro-26-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)- Methyl esterBethanecholCalcium Channel BlockersRatsCalcium Channel AgonistsEndocrinologyApaminMechanism of actionQuinolinesExcitatory postsynaptic potentialBiophysicsPyrazolesCalciummedicine.symptomMuscle Contractionmedicine.drugMuscle contractionNeurotensinEuropean Journal of Pharmacology
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Receptor phosphorylation does not mediate cross talk between muscarinic M(3) and bradykinin B(2) receptors.

1999

This study examined cross talk between phospholipase C-coupled muscarinic M3and bradykinin B2receptors coexpressed in Chinese hamster ovary (CHO) cells. Agonists of either receptor enhanced phosphoinositide signaling (which rapidly desensitized) and caused protein kinase C (PKC)-independent, homologous receptor phosphorylation. Muscarinic M3but not bradykinin B2receptors were also phosphorylated after phorbol ester activation of PKC. Consistent with this, muscarinic M3receptors were phosphorylated in a PKC-dependent fashion after bradykinin B2receptor activation, but muscarinic M3receptor activation did not influence bradykinin B2receptor phosphorylation. Despite heterologous phosphorylatio…

Atropinemedicine.medical_specialtyReceptor Bradykinin B2PhysiologyGene ExpressionCHO CellsInositol 145-TrisphosphateMuscarinic AntagonistsBiologyMuscarinic AgonistsBradykininTransfectionTritiumInternal medicineCricetinaeMuscarinic acetylcholine receptor M5Muscarinic acetylcholine receptormedicineMuscarinic acetylcholine receptor M4AnimalsHumansBradykinin receptorPhosphorylationReceptorMethacholine ChlorideReceptor Muscarinic M3Receptors BradykininMuscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2Cell BiologyMuscarinic acetylcholine receptor M1Receptor Cross-TalkReceptors MuscarinicRecombinant ProteinsEndocrinologyType C PhospholipasesCalciumInositolSignal TransductionThe American journal of physiology
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The non-neuronal cholinergic system in peripheral blood cells: Effects of nicotinic and muscarinic receptor antagonists on phagocytosis, respiratory …

2007

Peripheral blood cells express the complete non-neuronal cholinergic system. For example synthesis of acetylcholine and nicotinic as well muscarinic receptors have been demonstrated in leucocytes isolated from human peripheral blood. In the present experiments mononuclear cells and granulocytes were isolated from the peripheral blood to investigate content and synthesis of acetylcholine as well as phenotypic functions like respiratory burst, phagocytosis and migration. Mononuclear cells (T-cells and monocytes) contained 0.36 pmol/10(6) cells acetylcholine, whereas acetylcholine content in granulocytes was 100-fold lower. Acetylcholine synthesis amounted to 23.2+/-4.7 nmol/mg protein/h and 2…

Atropinemedicine.medical_specialtyTubocurarineMuscarinic AntagonistsNicotinic AntagonistsBiologyHexamethoniumGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundPhagocytosisCell MovementInternal medicineMuscarinic acetylcholine receptorMuscarinic acetylcholine receptor M4medicineHumansGeneral Pharmacology Toxicology and PharmaceuticsChromatography High Pressure LiquidRespiratory BurstNeuronsDose-Response Relationship DrugMuscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2General MedicineMuscarinic acetylcholine receptor M1BungarotoxinsAcetylcholineEndocrinologyNicotinic agonistchemistryLeukocytes MononuclearHexamethoniumAcetylcholineGranulocytesmedicine.drugLife Sciences
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The effects of histamine on the isolated mouse uterus

2000

1. A study is made of the contractile and relaxant effects, and mechanism of action, of histamine on isolated uterus from mice treated with diethylstilboestrol, employing acetylcholine and adrenaline as contractile and relaxant standard agents. 2. Concentration-response curves for histamine agonists were obtained in the absence and presence of selective histaminergic blocking drugs (clemizole, ranitidine and thioperamide) and indomethacin. A number of experiments were carried out in uterus from reserpinised mice. Concentration-response curves for acetylcholine and adrenaline were also obtained in the absence and presence of their selective antagonist (atropine and propranolol). 3. In isolat…

Atropinemedicine.medical_specialtyVasodilator AgentsHistamine AntagonistsHistamine agonistHistamine AgonistsRanitidineMiceUterine Contractionchemistry.chemical_compoundInternal medicinemedicineAnimalsDrug InteractionsDiethylstilbestrolPharmacologyThioperamideDose-Response Relationship DrugChemistryGeneral NeuroscienceUterusHistaminergicParasympatholyticsAcetylcholineClemizoleAtropineEndocrinologyFemaleAcetylcholineHistamineHistaminemedicine.drugJournal of Autonomic Pharmacology
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Absence of muscarinic modulation of vasopressin release from the isolated rat neurohypophysis

1975

1. Isolated rat neurohypophyses were incubated in Locke solution at 37°C and the vasopressin output into the medium determined by bioassay. 2. Potassium chloride 60 mM caused a 9-fold increase in the rate of vasopressin release that was abolished when calcium chloride was omitted from the Locke solution. 3. Acetylcholine 5.5×10−4 M neither alone nor in the presence of atropine 2.9×10−6 M changed the “resting” release of vasopressin. 4. Neither acetylcholine 5.5×10−4 M nor oxotremorine 10−4 and 3×10−4 M altered the vasopressin release evoked by potassium chloride 60 mM. 5. In contrast to the peripheral adrenergic nerve fibres, the secretory terminal fibres of the neurohypophysis do not appea…

Atropinemedicine.medical_specialtyVasopressinVasopressinschemistry.chemical_elementIn Vitro TechniquesCalciumInhibitory postsynaptic potentialPotassium ChloridePituitary Gland PosteriorInternal medicineMuscarinic acetylcholine receptormedicineOxotremorineAnimalsPharmacologyNeurosecretionChemistryOxotremorineGeneral MedicineAcetylcholineRatsAtropineEndocrinologyNicotinic agonistParasympathomimeticsCalciumFemaleAcetylcholinemedicine.drugNaunyn-Schmiedeberg's Archives of Pharmacology
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Involvement of PAR-4 in Cannabinoid-Dependent Sensitization of Osteosarcoma Cells to TRAIL-Induced Apoptosis

2014

The synthetic cannabinoid WIN 55,212-2 is a potent cannabinoid receptor agonist with anticancer potential. Experiments were performed to determine the effects of WIN on proliferation, cell cycle distribution, and programmed cell death in human osteosarcoma MG63 and Saos-2 cells. Results show that WIN induced G2/M cell cycle arrest, which was associated with the induction of the main markers of ER stress (GRP78, CHOP and TRB3). In treated cells we also observed the conversion of the cytosolic form of the autophagosome marker LC3-I into LC3-II (the lipidated form located on the autophagosome membrane) and the enhanced incorporation of monodansylcadaverine and acridine orange, two markers of t…

AutophagosomeautophagyProgrammed cell deathCannabinoids ER stress autophagy TRAIL osteosarcoma cells GRP78/PAR-4 complex.Cannabinoid receptorMorpholinesCellApoptosisTRAILNaphthalenesBiologyGRP78/PAR-4 complex.Applied Microbiology and BiotechnologyTNF-Related Apoptosis-Inducing LigandCadaverineCell Line TumorSettore BIO/10 - BiochimicamedicineHumansRNA Small InterferingEndoplasmic Reticulum Chaperone BiPMolecular BiologyHeat-Shock ProteinsEcology Evolution Behavior and SystematicsCell ProliferationCannabinoid Receptor AgonistsOsteosarcomaCannabinoidsAutophagyCell Cycle Checkpointsosteosarcoma cellsCell BiologyCell cycleEndoplasmic Reticulum StressAcridine OrangeBenzoxazinesCell biologymedicine.anatomical_structureApoptosisAutophagosome membraneApoptosis Regulatory ProteinsER stressMicrotubule-Associated ProteinsResearch PaperDevelopmental Biology
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Antagonism of the endophytic Bacillus subtilis strain AG1 to fungal pathogens that cause tracheomycotic deterioration of wine wood

2008

Grapevine trunk diseases can determine considerable losses in the worldwide wine industry. Symptoms of wood diseases are dead spurs, arms, cordons and same times vine death, due to cankers in the vascular tissue (Pascoe, 2000). Recent research has also showed a recrudescence either of escadisease or decay by Verticilliumdahliae and the occurrence of new wood alterations (Botryosphaeriarhodina; Mugnai et al., 1999; Wood et al., 2005; Bonfiglioliet al., 2007). Last investigations, carried out in Sicilian vineyards on fungi associated with xilematic“esca”symptoms, revealed the occurrence of genus Bacillusin wood tissues. A spore-producer Gram-positive bacterial isolate, named AG1, was identifi…

BACILLUS SUBTILIS ESCA FUNGI ANTAGONISM
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