Search results for "Mollusk Venoms"

showing 2 items of 2 documents

Differential blockade by nifedipine and ω-conotoxin GVIA of α1- and β1-adrenoceptor-controlled calcium channels on motor nerve terminals of the rat

1990

Electrically evoked release of [3H]acetylcholine ([3H]ACh) from the rat phrenic nerve and its facilitation by stimulation of presynaptic alpha 1- and beta 1-adrenoceptors were investigated in the absence and presence of nifedipine and omega-conotoxin GVIA. Both calcium channel antagonists did not modify electrically evoked [3H]ACh release, but selectively blocked the effect triggered by both facilitatory adrenergic receptors. The increase in [3H]ACh release mediated via beta 1-adrenoceptor activation was abolished by low concentrations (1 nM) of omega-conotoxin GVIA, whereas nifedipine (100 nM) abolished the facilitatory effect mediated via alpha 1-adrenoceptor stimulation. Therefore, the b…

medicine.medical_specialtyNifedipineNeuromuscular JunctionMollusk Venomschemistry.chemical_elementIn Vitro TechniquesCalciumN-type calcium channelMotor Endplatecomplex mixturesNeuromuscular junctionNifedipineomega-Conotoxin GVIAInternal medicinemedicineAnimalsL-type calcium channelVoltage-dependent calcium channelChemistryGeneral NeuroscienceCalcium channelRats Inbred StrainsCalcium Channel BlockersAcetylcholineElectric StimulationRatsReceptors AdrenergicPhrenic Nervemedicine.anatomical_structureEndocrinologyCalcium ChannelsAcetylcholinemedicine.drugNeuroscience Letters
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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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