Search results for "Charybdotoxin"

showing 10 items of 15 documents

Endothelium-dependent responses in human isolated thyroid arteries from donors

2004

The functional properties of the endothelium of human thyroid arteries remain unexplored. We investigated the intervention of nitric oxide (NO), prostacyclin (PGI(2)) and endothelium-derived hyperpolarizing factor (EDHF) in the responses to acetylcholine and noradrenaline in isolated thyroid arteries obtained from multi-organ donors. Artery rings were suspended in organ baths for isometric recording of tension. The contribution of NO, PGI(2) and EDHF to endothelium-dependent relaxation was determined by the inhibitory effects of N(G)-monomethyl-L-arginine (L-NMMA), indomethacin, and K(+) channel inhibitors respectively. Acetylcholine induced concentration-dependent relaxation; this effect w…

AdultMalemedicine.medical_specialtyCharybdotoxinCharybdotoxinEndotheliumEndocrinology Diabetes and MetabolismIndomethacinThyroid GlandProstacyclinNitric OxideApaminOuabainNitric oxideBiological FactorsNorepinephrinechemistry.chemical_compoundEndocrinologyCulture TechniquesInternal medicinePotassium Channel BlockersmedicineHumansomega-N-MethylarginineDose-Response Relationship DrugArteriesMiddle AgedEpoprostenolAcetylcholineEndocrinologymedicine.anatomical_structureApaminchemistryVasoconstrictioncardiovascular systemFemaleEndothelium VascularNitric Oxide SynthaseSodium-Potassium-Exchanging ATPasePeptidesAcetylcholinemedicine.drugArteryJournal of Endocrinology
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Modulation of adrenergic responses of human vas deferens by K+ channel inhibitors.

2010

Objectives The present study was designed to evaluate the role of K + channels in the adrenergic responses of human vas deferens as well as the intervention of dihydropyridine-sensitive Ca 2+ channels on modulation of adrenergic responses by K + channel inhibitors. Methods Ring segments of the epididymal part of the vas deferens were taken from 32 elective vasectomies and mounted in organ baths for isometric recording of tension. We then studied the effects of K + channel blockers on neurogenic and norepinephrine-induced contractile responses. Results Addition of tetraethylammonium (TEA, 10 −3 M), a nonspecific K + channel blocker, or charybdotoxin (10 −7 M), a nonselective inhibitor of lar…

AdultMalemedicine.medical_specialtyPotassium ChannelsCharybdotoxinCalcium Channels L-TypeCharybdotoxinNifedipineUrologyAdrenergicApaminGlibenclamidechemistry.chemical_compoundNorepinephrineVas DeferensNifedipineInternal medicineReceptors Adrenergic alpha-1GlyburidePotassium Channel BlockersMedicineHumansChannel blockerTetraethylammoniumIon Transportbusiness.industryVas deferensTetraethylammoniumMuscle SmoothElectric StimulationEndocrinologymedicine.anatomical_structurechemistryApaminPotassiumCalciumbusinessPeptidesmedicine.drugMuscle ContractionUrology
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Nitric oxide mediates abnormal responsiveness of thyroid arteries in methimazole-treated patients.

2005

Objective: We studied the intervention of nitric oxide (NO), prostacyclin and endothelium-derived hyperpolarizing factor (EDHF) in mediating responses to acetylcholine in thyroid arteries from euthyroid and methimazole-treated (MT) patients. Design and methods: Branches of the superior thyroid artery were obtained from 19 euthyroid patients and 17 MT patients (euthyroid at the time of surgery) undergoing total thyroidectomy or hemithyroidectomy. Artery rings were suspended in organ baths for isometric recording of tension. Results and conclusions: Acetylcholine caused endothelium-dependent relaxation of greater magnitude in arteries from MT patients (pD2 (−log EC50) values were 7.68±0.19 in…

AdultMalemedicine.medical_specialtyPotassium ChannelsCharybdotoxinEndocrinology Diabetes and MetabolismMuscle RelaxationThyroid GlandApaminNitric OxideHyperthyroidismMuscle Smooth VascularSuperior thyroid arterychemistry.chemical_compoundBiological FactorsNorepinephrineEndocrinologyAntithyroid AgentsInternal medicinemedicine.arterymedicinePotassium Channel BlockersHumansEuthyroidEnzyme InhibitorsMethimazoleomega-N-Methylargininebusiness.industryThyroidGeneral MedicineArteriesMiddle AgedAcetylcholinemedicine.anatomical_structureEndocrinologychemistryApaminCirculatory systemPotassiumCalciumFemaleEndothelium VascularNitric Oxide SynthasebusinessAcetylcholinemedicine.drugBlood vesselArteryEuropean journal of endocrinology
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Role of NO-synthases and cyclooxygenases in the hyperreactivity of male rabbit carotid artery to testosterone under experimental diabetes.

2009

Abstract Cardiovascular disease is the major cause of morbidity and mortality in diabetic patients, which in turn is also associated with low levels of serum testosterone. The working hypothesis was that diabetes might modify the mechanisms involved in the vascular actions of testosterone in isolated rabbit carotid arteries. Testosterone (10 −8 –3 × 10 −4  M) induced a concentration-dependent relaxation of precontracted carotid arteries, which was higher in diabetic than in control rabbits. In control rabbits neither endothelium removal nor the nitric oxide synthase (NOS) inhibitor N G -nitro- l -arginine ( l -NOArg, 10 −5  M) modified the relaxant action of testosterone, and the cyclooxyge…

Blood GlucoseCarotid Artery DiseasesMalemedicine.medical_specialtyArginineEndotheliumCharybdotoxinNitric Oxide Synthase Type IIIThromboxaneBlotting WesternIndomethacinNitric Oxide Synthase Type IIVasodilationProstacyclinNitric OxideNitroarginineDiabetes Mellitus ExperimentalImmunoenzyme TechniquesThromboxane A2Internal medicinemedicinePotassium Channel BlockersAnimalsCyclooxygenase InhibitorsTestosteronePharmacologybiologyDose-Response Relationship Drugbusiness.industryTestosterone (patch)EpoprostenolNitric oxide synthaseVasodilationEndocrinologymedicine.anatomical_structureCarotid ArteriesApaminCyclooxygenase 2cardiovascular systembiology.proteinPotassiumCalciumCyclooxygenaseEndothelium VascularRabbitsbusinessDiabetic Angiopathiesmedicine.drugPharmacological research
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Potassium channels contribute to the increased sensitivity of the rabbit carotid artery to hydrogen sulfide in diabetes

2019

Abstract Hydrogen sulfide (H2S) is a potential endothelium-derived hyperpolarizing factor (EDHF) and adventitium- or adipocyte-derived relaxing factor (ADRF) which vasorelaxant action is mediated by potassium channels. H2S could also play an important role in the pathophysiology of diabetic cardiovascular complications. The present study has investigated the influence of alloxan-induced diabetes on the role of potassium channels mediating the relaxant response of the rabbit carotid artery to NaHS, a donor of H2S. NaHS (10−8-3 × 10−5 M) relaxed phenylephrine-precontracted carotid arteries, with higher potency in diabetic than in control rabbits. The selective blockers of potassium channels c…

Male0301 basic medicinePotassium ChannelsCharybdotoxinCarotid arteriesHydrogen sulfidePharmacologyPotassium channelsDiabetes Mellitus ExperimentalGlibenclamide03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDiabetes mellitusmedicineAnimalsHydrogen SulfidePharmacologyHydrogen sulfideDose-Response Relationship DrugChemistryDiabetesmedicine.diseasePathophysiologyPotassium channelVasodilationCarotid Arteries030104 developmental biologyRabbitsCarotid artery030217 neurology & neurosurgerymedicine.drugEuropean Journal of Pharmacology
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Involvement of K+ channels in the relaxant effects of YC-1 in vascular smooth muscle

1999

This study addresses the question whether K(+) channels are involved in the vasorelaxant effects of 3-(5'-hydroxymethyl-2'-furyl)-1-benzyl-indazole (YC-1 ). In rat aorta, guinea pig aorta, and guinea pig a. carotis, YC-1 inhibited contractions induced by phenylephrine (3 microM) more potently than those induced by K(+)(48 mM). In rat aorta, tetraethylammonium (10 mM), charybdotoxin (0.2 microM), and iberiotoxin (0.1 microM), but not glibenclamide (10 microM), attenuated the relaxant effects of YC-1. In guinea pig a. carotis, YC-1 (30 microM) induced a hyperpolarisation which was antagonised by 1H-[1,2,4]oxadiazolo[4, 3-a]quinoxalin-1-one (ODQ; 50 microM). In rat aorta, YC-1 (30 microM) incr…

MaleIndazolesPotassium ChannelsTime FactorsVascular smooth muscleCharybdotoxinMuscle RelaxationGuinea PigsAorta ThoracicIn Vitro TechniquesPharmacologyMuscle Smooth VascularMembrane PotentialsRats Sprague-DawleyGlibenclamidePhenylephrinechemistry.chemical_compoundmedicine.arterymedicineAnimalsDrug InteractionsPhenylephrinePharmacologyAortaTetraethylammoniumDose-Response Relationship DrugChemistryAnatomyIberiotoxinRatsVasodilationCarotid ArteriesPotassiumFemaleZaprinastmedicine.drugEuropean Journal of Pharmacology
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Role of Ca2+-Activated K+ Channels on Adrenergic Responses of Human Saphenous Vein

2006

Background We studied the participation of K + channels on the adrenergic responses in human saphenous veins as well as the intervention of dihydropyridine-sensitive Ca 2+ channels on modulation of adrenergic responses by K + channels blockade. Methods Saphenous vein rings were obtained from 40 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. Results Iberiotoxin (10 −7 mol/L), an inhibitor of large conductance Ca 2+ -activated K + channels, and charybdotoxin (10 −7 mol/L), an inhibitor of both large and intermediate conductance Ca 2+ -activated K + channels, enhanced the contractions elicited by elec…

MaleNifedipineCharybdotoxinAdrenergicStimulationIn Vitro TechniquesApaminMuscle Smooth VascularNorepinephrinePotassium Channels Calcium-Activatedchemistry.chemical_compoundInternal MedicinemedicineHumansSaphenous VeinChannel blockerbusiness.industryDihydropyridineMiddle AgedIberiotoxinCalcium Channel BlockersElectric StimulationchemistryVasoconstrictionMuscle TonusAnesthesiaBiophysicsFemalemedicine.symptombusinessMuscle contractionmedicine.drugAmerican Journal of Hypertension
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Mechanisms underlying the nitric oxide inhibitory effects in mouse ileal longitudinal muscle

2005

We investigated the mechanisms involved in the nitric oxide (NO)-induced inhibitory effects on longitudinal smooth muscle of mouse ileum, using organ bath technique. Exogenously applied NO, delivered as sodium nitroprusside (SNP; 0.1–100 µmol/L) induced a concentration-dependent reduction of the ileal spontaneous contractions. 1H-[1,2,4]oxadiazolol[4,3,a]quinoxalin-1-one (ODQ; 1 µmol/L), a guanilyl cyclase inhibitor, reduced the SNP-induced effects. Tetraethylammonium chloride (20 mmol/L), a non-selective K+ channel blocker, and charybdotoxin (0.1 µmol/L), blocker of large conductance Ca2+-dependent K+ channels, significantly reduced SNP-induced inhibitory effects. In contrast, apamin (0.1…

MaleNitroprussideThapsigarginCharybdotoxinPhysiologyMouse ileumIn Vitro TechniquesPharmacologyApaminSettore BIO/09 - FisiologiaPotassium channelsMicePotassium Channels Calcium-Activatedchemistry.chemical_compoundIleumPhysiology (medical)Cyclic GMP-Dependent Protein KinasesPotassium Channel BlockersmedicineAnimalsNitric Oxide DonorsChannel blockerCyclic GMPPharmacologyRyanodineRyanodine receptorCalcium storeMuscle SmoothPotassium channel blockerNitric oxideGeneral MedicineTetraethylammonium chlorideMice Inbred C57BLchemistryCalciumSodium nitroprussideMuscle ContractionSignal Transductionmedicine.drug
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Components of after-hyperpolarization in magnocellular neurones of the rat supraoptic nucleusin vitro

1998

1. The pharmacological sensitivity of hyperpolarizing components of spike train after-potentials was examined in sixty-one magnocellular neurones of the rat supraoptic nucleus using intracellular recording techniques in a brain slice preparation. 2. In 26 % of all neurones a slow after-hyperpolarization (AHP) was observed in addition to a fast AHP. In 31 % of all neurones a depolarizing after-potential (DAP) was observed. 3. The fast AHP was blocked by apamin whereas the slow AHP was blocked by charybdotoxin (ChTX). The DAP was enhanced by ChTX or a DAP was unmasked if not present during the control period. 4. Low concentrations of TEA (0.15-1.5 mM) induced effects on the slow AHP and the D…

MalePotassium ChannelsCharybdotoxinPhysiologySpike trainAction PotentialsApaminSupraoptic nucleusRats Sprague-DawleySK channelchemistry.chemical_compoundSlice preparationAnimalsNeuronsKv1.3 Potassium ChannelVoltage-gated ion channelChemistryMargatoxinTetraethylammoniumOriginal ArticlesIberiotoxinImmunohistochemistryRatsElectrophysiologyApaminPotassium Channels Voltage-GatedBiophysicsSupraoptic NucleusNeuroscienceThe Journal of Physiology
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The Janus face of chlorogenic acid on vascular reactivity: A study on rat isolated vessels

2016

Abstract Background Chlorogenic acid (CGA), the main polyphenol contained in coffee, is a major contributor to dietary polyphenol intake. Few studies reported its anti-hypertensive properties but the mechanisms are still indefinite. Purpose The present study assessed the direct effect of CGA in endothelium denuded or intact aortic rings from male Wistar rats and the mechanisms involved. Methods/Results CGA induced a direct endothelium-dependent relaxation that was significantly reduced by L-NAME (10 −4  M), indomethacin (10 −5  M) and combination of apamin (10 −7  M) and charybdotoxin (10 −7  M). Incubation of rings with CGA induced a dual effect on agonist-induced vasorelaxation. At 10 −6 …

Maleendocrine systemCharybdotoxinEndotheliumPharmaceutical ScienceVasodilation030204 cardiovascular system & hematologyPharmacologyApaminMuscle Smooth Vascular03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDrug DiscoverymedicineAnimals[CHIM]Chemical SciencesRats WistarPhenylephrineAntihypertensive AgentsComputingMilieux_MISCELLANEOUSPharmacology[SDV.SP]Life Sciences [q-bio]/Pharmaceutical sciencesRatsVasodilationmedicine.anatomical_structureComplementary and alternative medicineBiochemistrychemistry030220 oncology & carcinogenesisHypertensionMolecular MedicineSodium nitroprussideEndothelium Vascularmedicine.symptomChlorogenic AcidVasoconstrictionAcetylcholinemedicine.drug
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