Search results for "Apamin"

showing 10 items of 39 documents

Chronic exercise impairs nitric oxide pathway in rabbit carotid and femoral arteries

2018

KEY POINTS: Some of the beneficial effects of exercise in preventing vascular related diseases are mediated by the enhancement of endothelial function where the role of nitric oxide (NO) is well documented, although the relevance of calcium activated potassium channels is not fully understood. The impact of oxidative stress induced by training on endothelial function remains to be clarified. By evaluating different endothelial vasodilator pathways on two vascular beds in a rabbit model of chronic exercise, we found a decreased NO bioavailability and endothelial nitric oxide synthase expression in both carotid and femoral arteries. Physical training induced carotid endothelial dysfunction as…

Male0301 basic medicinemedicine.medical_specialtyPhysiologyVasodilationFemoral artery030204 cardiovascular system & hematologyNitric OxideApaminNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEnosPhysical Conditioning AnimalInternal medicinemedicine.arterymedicineAnimalsLarge-Conductance Calcium-Activated Potassium ChannelsEndothelial dysfunctionExercisebiologybiology.organism_classificationmedicine.diseaseCalcium-activated potassium channelFemoral ArteryOxidative StressCarotid Arteries030104 developmental biologyEndocrinologychemistryNitric Oxide PathwayEndothelium VascularRabbitsThe Journal of Physiology
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Neurotransmitters involved in the fast inhibitory junction potentials in mouse distal colon

2003

We investigated, in murine colon circular muscle, the role of adenosine 5′-triphosphate (ATP) and pituitary adenylate cyclase activating peptide (PACAP) as inhibitory neurotransmitters of the fast component of nerve-evoked inhibitory junction potential (fast IJP). Fast IJP was antagonised by apamin or suramin, abolished by desensitisation with the P2Y receptor agonist, adenosine 5′-O-2-thiodiphosphate (ADPβS), unaffected by desensitisation with P2X receptor agonist, α,β-methylene ATP (α,β-meATP), and reduced by PACAP-(6-38), a PACAP receptor antagonist. ATP induced membrane hyperpolarization resistant to tetrodotoxin, Nω-nitro-L-arginine methyl ester (L-NAME) or PACAP-(6-38), but antagonise…

MaleAgonistendocrine systemmedicine.medical_specialtyP2Y receptorColonmedicine.drug_classPurinoceptorNeuromuscular JunctionSuraminTetrodotoxinBiologyApaminSettore BIO/09 - FisiologiaMembrane PotentialsCellular and Molecular NeuroscienceMicechemistry.chemical_compoundAdenosine TriphosphateInternal medicinemedicineAnimalsMurinePharmacologyNeurotransmitter AgentsDose-Response Relationship Drugmusculoskeletal neural and ocular physiologyNeuropeptidesMembrane hyperpolarizationThionucleotidesHyperpolarization (biology)Receptor antagonistAdenosinePeptide FragmentsATPAdenosine DiphosphatePituitary adenylate cyclase-activating peptideNG-Nitroarginine Methyl EsterEndocrinologyApaminchemistryPituitary Adenylate Cyclase-Activating PolypeptideFast inhibitory junction potentialPACAP (pituitary adenylate cyclase activating peptide)hormones hormone substitutes and hormone antagonistsmedicine.drugEuropean Journal of Pharmacology
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Mechanisms underlying the inhibitory effects induced by pituitary adenylate cyclase-activating peptide in mouse ileum

2005

Abstract The aim of this study was to investigate the signal transduction mechanisms underlying the inhibitory effect induced by pituitary adenylate cyclase activating peptide (PACAP-27) on the spontaneous contractile activity of longitudinal muscle of mouse ileum. Mechanical activity of ileal segments was recorded isometrically in vitro. PACAP-27 produced apamin-sensitive reduction of the amplitude of the spontaneous contractions. 9-(Tetrahydro-2-furanyl)-9H-purin-6-amine (SQ 22,536), adenylate cyclase inhibitor, or genistein and tyrphostin 25, tyrosine kinase inhibitors, had negligible effects on PACAP-27-induced inhibition. PACAP-27 effects were significantly inhibited by U-73122, phopho…

MaleIndolesPhosphodiesterase InhibitorsVasodilator AgentsMouse ileumStimulationSettore BIO/09 - FisiologiaMicechemistry.chemical_compoundInositolEnzyme InhibitorsEstrenesRyanodineRyanodine receptorProtein-Tyrosine KinasesTyrphostinsGenisteinPyrrolidinonesCell biologyPituitary adenylate cyclase-activating peptideNG-Nitroarginine Methyl EsterPituitary Adenylate Cyclase-Activating PolypeptideThapsigarginSignal transductionCyclopiazonic acidhormones hormone substitutes and hormone antagonistsMuscle ContractionBoron Compoundsendocrine systemmedicine.medical_specialtyThapsigarginMuscular inhibitionCalcium-Transporting ATPasesIn Vitro TechniquesInositol 145-triphosphateBiologyPACAP-27 (pituitary adenylate cyclase activating peptide)IleumPhospholipase CInternal medicinemedicineAnimalsPharmacologyDose-Response Relationship DrugPhospholipase CAdenineMuscle SmoothMice Inbred C57BLEndocrinologyApaminchemistryAdenylyl Cyclase InhibitorsCalciumNitric Oxide SynthaseEuropean Journal of Pharmacology
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Inhibitory effect of caffeic acid phenethyl ester, a plant-derived polyphenolic compound, on rat intestinal contractility

2009

Abstract Caffeic acid phenethyl ester (CAPE) exerts pharmacological actions (e.g. anti-inflammatory, chemopreventive) which are relevant for potential clinical application in the digestive tract. However, no study has been published on its possible effects on intestinal motility, to date. In the present study, we investigated the effect of this plant-derived polyphenolic compound on the spontaneous contractions of the rat isolated ileum. CAPE reduced (in a tetrodotoxin-insensitive manner) spontaneous ileal contractions and this effect was reduced by the l -type Ca 2+ channel blocker nifedipine and the chelant of calcium ethylenediaminetetraacetic acid. However, the effect of CAPE was not mo…

MaleMuscle Relaxationchemistry.chemical_elementPharmacologyCalciumIn Vitro TechniquesApaminPotassium Chloridechemistry.chemical_compoundPhentolamineCaffeic AcidsPhenolsIleumCaffeic acidmedicineAnimalsChannel blockerRats WistarCaffeic acid phenethyl esterPharmacologyFlavonoidsVoltage-dependent calcium channelPolyphenolsPhenylethyl AlcoholPlantsRatschemistryBiochemistryCyclopiazonic acidmedicine.drugMuscle Contraction
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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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Nitric oxide induces muscular relaxation via cyclic GMP-dependent and -independent mechanisms in the longitudinal muscle of the mouse duodenum

2003

The aim of this study was to investigate, in mouse duodenum, the role of nitric oxide (NO) in the relaxation of longitudinal muscle evoked by nerve activation and the coupled action mechanism. Electrical field stimulation (EFS; 0.5ms, 10-s train duration, supramaximal voltage, at various frequencies) under nonadrenergic noncholinergic conditions evoked muscular relaxation occasionally followed, at the higher stimulus frequencies, by rebound contractions. Inhibition of the synthesis of NO by Nω-nitro-L-arginine methyl ester (L-NAME; 100μM) virtually abolished the evoked relaxation. The relaxation was reduced also by apamin (0.1μM) and by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 1μM)…

MaleNitroprussideCancer Researchmedicine.medical_specialtyPotassium ChannelsDuodenumPhysiologyMuscle RelaxationClinical BiochemistryNonadrenergic noncholinergic relaxationStimulationStimulus (physiology)Inhibitory postsynaptic potentialApaminSettore BIO/09 - FisiologiaBiochemistryNitric oxideMicechemistry.chemical_compoundInternal medicineK+ -channelmedicineAnimalsCyclic GMPMolecular BiologyDose-Response Relationship DrugMuscle SmoothNitric oxideElectric StimulationDose–response relationshipEndocrinologychemistryTetrodotoxinSodium nitroprussideMouse duodenummedicine.drugNitric Oxide
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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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Nitrergic and purinergic interplay in inhibitory transmission in rat gastric fundus.

2007

Summary 1  This study was undertaken to analyse the involvement of ATP in non-adrenergic non- cholinergic (NANC) relaxation and possible interplay between nitrergic and purinergic systems in rat gastric fundus. 2  Experiments were performed in vitro on strips of longitudinal muscle from rat gastric fundus, recording the mechanical activity as changes in isometric force. In addition, NO release induced by different experimental conditions was assayed. 3  Under NANC conditions in serotonin-precontracted strips, electrical field stimulation (EFS) elicited a tetrodotoxin (TTX)-sensitive relaxation accompanied by nitric oxide (NO) release. This effect was antagonized by pretreatment with the NO …

MaleNitroprussidemedicine.medical_specialtyAdenosineMuscle RelaxationStimulationTetrodotoxinIn Vitro TechniquesInhibitory postsynaptic potentialApaminNitric OxideNitroargininechemistry.chemical_compoundAdenosine TriphosphateDesensitization (telecommunications)Internal medicineNitrergic NeuronsmedicineAnimalsNitric Oxide DonorsGastric FundusEnzyme InhibitorsRats WistarPharmacologyPurinergic receptorReceptors PurinergicMuscle SmoothAdenosine MonophosphateElectric StimulationRatsAdenosine DiphosphateEndocrinologychemistryApaminTetrodotoxinCholinergicFemaleSodium nitroprussideNitric Oxide Synthasemedicine.drugAutonomicautacoid pharmacology
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Inhibitory purinergic transmission in mouse caecum: Role for P2Y1 receptors as prejunctional modulators of ATP release

2007

Using conventional microelectrode recording techniques, we investigated, in the circular muscle of the mouse caecum, the neurotransmitter(s) involved in the neurally-evoked inhibitory junction potentials (IJPs) and the existence of possible prejunctional mechanisms controlling neurotransmitter release. Electrical field stimulation with single pulses elicited IJPs, consisting only of a "fast" hyperpolarization, while using train stimuli (30-50 Hz) the initial fast hyperpolarization was followed by a slower hyperpolarization. The fast and the slow component were selectively antagonized by apamin, a blocker of calcium-activated potassium channels, and N(omega)-nitro-l-arginine methyl ester (l-…

MaleP2Y receptormedicine.medical_specialtyAntineoplastic AgentsSuraminNitric OxideApaminSettore BIO/09 - FisiologiaSynaptic TransmissionEnteric Nervous SystemMembrane PotentialsMiceReceptors Purinergic P2Y1chemistry.chemical_compoundAdenosine TriphosphateInternal medicinePurinergic P2 Receptor AntagonistsmedicineAnimalsPPADSReceptorCecumMembrane potentialReceptors Purinergic P2General NeurosciencePurinergic receptorMembrane ProteinsHyperpolarization (biology)Electric StimulationReceptors Purinergic P2Y12Potassium channelMice Inbred C57BLEndocrinologyApaminchemistryBiophysicsenteric nerves intestinal muscle ATP purinergic receptors inhibitory junction potentialsNeuroscience
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Mechanisms underlying hyperpolarization evoked by P2Y receptor activation in mouse distal colon

2006

In murine colonic circular muscle, ATP mediates fast component of the nerve-evoked inhibitory junction potentials, via activation of P2Y receptors and opening of apamin-sensitive Ca2+-dependent K+ channels. We investigated, using microelectrode recordings, the intracellular events following P2Y-receptor activation by electrical field stimulation or by adenosine 5'-O-2-thiodiphosphate (ADPbetaS), ATP stable analogue. The fast-inhibitory junction potential amplitude was reduced by thapsigargin or ciclopiazonic acid (CPA), sarcoplasmic reticulum Ca2+-ATPase inhibitors, by ryanodine, which inhibits Ca2+ release from ryanodine-sensitive stores, and by 9-(tetrahydro-2-furanyl)-9H-purin-6-amine (S…

MaleP2Y receptormedicine.medical_specialtyThapsigarginColonMouse colonBiologyApaminSettore BIO/09 - FisiologiaEnteric inhibitory neurotransmissionAdenylyl cyclaseMicePotassium Channels Calcium-Activatedchemistry.chemical_compoundIntracellular microelectrode recordingReceptors Adrenergic alpha-1Internal medicinemedicineAnimalsCalcium-dependent potassium channelNeuronsPharmacologyModels StatisticalForskolinDose-Response Relationship DrugReceptors Purinergic P2Ryanodine receptorColforsinCalcium storeP2Y receptorHyperpolarization (biology)Inositol trisphosphate receptorElectrophysiologyMice Inbred C57BLEndocrinologychemistryBiophysicsCalciumAdenylyl CyclasesEuropean Journal of Pharmacology
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