Search results for " calcium channel"

showing 4 items of 64 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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Vascular effects of progesterone: Role of cellular calcium regulation

2001

Abstract —Vascular actions of progesterone have been reported, independently of estrogen, affecting both blood pressure and other aspects of the cardiovascular system. To study possible mechanisms underlying these effects, we examined the effects of P in vivo in intact rats and in vitro in isolated artery and vascular smooth muscle cell preparations. In anesthetized Sprague-Dawley rats , bolus intravenous injections of P (100 μg/kg) significantly decreased pressor responses to norepinephrine (0.3 μg/kg). In vitro, progesterone (10 −8 to 10 −5 mmol/L) produced a significant, dose-dependent relaxation of isolated helical strips, both of rat tail artery precontracted with KCl (60 mmol/L) or a…

medicine.medical_specialtyVasopressinVascular smooth musclemedicine.drug_classchemistry.chemical_elementBiologyCalciumCalcium in biologyNorepinephrine (medication)EndocrinologychemistryEstrogenInternal medicineCirculatory systemInternal MedicinemedicineL-type calcium channelmedicine.drug
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MECHANISMS OF TENSION DEVELOPMENT INDUCED BY MONENSIN IN GUINEA-PIG AORTA : EFFECTS OF VERAPAMIL, OUABAIN, PRAZOSIN AND GLIBENCLAMIDE

1993

The influence of monensin (10 µmol/L) alone and in the presence of verapamil (3 µmol/L) or ouabain (1 mmol) and prazosin (1 µmol/L) or glibenclamide (10 µmol/L) were studied on the muscle tension of guinea pig aorta. Changes in tissue sodium, potassium and calcium ion contents of the aortic muscle produced by monensin in the presence of prazosin were evaluated. Monensin in normal Tyrode's solution containing prazosin caused an increase in the resting tension followed by a decrease and returned to normal values. Verapamil reduced the muscle tension induced by monensin. After ouabain, monensin induced sustained increase in the resting tension. Glibenclamide partially reversed the relaxant pha…

medicine.medical_specialtyanimal structuresVoltage-dependent calcium channelChemistryMonensinchemistry.chemical_elementCalciumOuabaincarbohydrates (lipids)Glibenclamidechemistry.chemical_compoundEndocrinologyMuscle tensionInternal medicinecardiovascular systemPrazosinmedicineVerapamilheterocyclic compoundsmedicine.drugZagazig Journal of Pharmaceutical Sciences
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Endothelin action on goat cerebral arteries.

1990

Abstract Cumulative application of endothelin-1 (human) markedly constricted goat isolated cerebral arteries in a concentration-dependent manner. Contractile responses were not affected by removal of endothelial cells. Removal of extracellular calcium or addition of the calcium channel blocker nicardipine (10−7 M) failed to abolish responses to endothelin. The results suggest that the endothelium-independent constriction of cerebral arteries produced by endothelin cannot be explained solely by voltage-dependent calcium channels. The contractile responses are likely to be mediated by stimulation of specific receptors for this peptide.

medicine.medical_specialtymedicine.drug_classCerebral arteriesNicardipinePharmaceutical Sciencechemistry.chemical_elementStimulationCalcium channel blockerBiologyCalciumIn Vitro TechniquesMuscle Smooth VascularNicardipineInternal medicinemedicineAnimalsPharmacologyVoltage-dependent calcium channelEndothelinsGoatsCerebral ArteriesEndocrinologymedicine.anatomical_structurechemistrycardiovascular systemCalciumFemaleEndothelium VascularEndothelin receptormedicine.drugBlood vesselMuscle ContractionThe Journal of pharmacy and pharmacology
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