Search results for "POTASSIUM CHANNELS"

showing 10 items of 94 documents

KCND3 potassium channel gene variant confers susceptibility to electrocardiographic early repolarization pattern

2019

BACKGROUND: The presence of an early repolarization pattern (ERP) on the surface ECG is associated with risk of ventricular fibrillation and sudden cardiac death. Family studies have shown that ERP is a highly heritable trait, but molecular genetic determinants are unknown. METHODS: To identify genetic susceptibility loci for ERP, we performed a GWAS and meta-analysis in 2,181 cases and 23,641 controls of European ancestry. RESULTS: We identified a genome-wide significant (P < 5 × 10(–8)) locus in the potassium voltage-gated channel subfamily D member 3 (KCND3) gene that was successfully replicated in additional 1,124 cases and 12,510 controls. A subsequent joint meta-analysis of the discov…

Male0301 basic medicineGenotypeHeart VentriclesGenome-wide association studyLocus (genetics)BiologyPolymorphism Single NucleotideWhite PeopleSudden cardiac deathElectrocardiography03 medical and health sciences0302 clinical medicineGenetic variationmedicineGenetic predispositionHumansSNPGWASGenetic Predisposition to DiseaseJ-POINT ELEVATIONS422LAlleleGENOME-WIDE ASSOCIATIONGeneMUTATIONAllelesMETAANALYSISGeneticsGeneral Medicinemedicine.diseaseddc:Death Sudden CardiacShal Potassium Channels030104 developmental biologyGenetic Loci030220 oncology & carcinogenesisVentricular FibrillationCORONARY-ARTERY-DISEASEFemaleVENTRICULAR-FIBRILLATIONClinical MedicineTranscriptomeGenome-Wide Association Study
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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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Inhibition of histone deacetylation rescues phenotype in a mouse model of Birk-Barel intellectual disability syndrome

2020

Mutations in the actively expressed, maternal allele of the imprinted KCNK9 gene cause Birk-Barel intellectual disability syndrome (BBIDS). Using a BBIDS mouse model, we identify here a partial rescue of the BBIDS-like behavioral and neuronal phenotypes mediated via residual expression from the paternal Kcnk9 (Kcnk9pat) allele. We further demonstrate that the second-generation HDAC inhibitor CI-994 induces enhanced expression from the paternally silenced Kcnk9 allele and leads to a full rescue of the behavioral phenotype suggesting CI-994 as a promising molecule for BBIDS therapy. Thus, these findings suggest a potential approach to improve cognitive dysfunction in a mouse model of an impri…

Male0301 basic medicinePotassium Channels[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyGeneral Physics and AstronomyDiseasePhenylenediamines[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyCraniofacial AbnormalitiesHistonesMice0302 clinical medicineIntellectual disabilityImprinting (psychology)lcsh:ScienceMice KnockoutGeneticsMultidisciplinaryBehavior AnimalbiologyNeurodevelopmental disordersDevelopmental disordersQBrainPhenotypeUp-RegulationPhenotypeHistoneGene Knockdown TechniquesBenzamidesMuscle HypotoniaFemaleLocus CoeruleusEpigeneticsScienceArticleGeneral Biochemistry Genetics and Molecular BiologyGenomic Imprinting03 medical and health sciencesDevelopmental disorders ; Neurodevelopmental disorders ; EpigeneticsIntellectual DisabilitymedicineAnimalsHumansddc:610AlleleGene[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Chemistrymedicine.diseaseHistone Deacetylase InhibitorsMice Inbred C57BLDisease Models Animal030104 developmental biologyAcetylationMutationbiology.proteinlcsh:Q030217 neurology & neurosurgery
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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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Endothelial and neural factors functionally involved in the modulation of noradrenergic vasoconstriction in healthy pig internal mammary artery

2011

The role of endothelial and neural factors as modulators of neurogenic- and noradrenaline-induced vasoconstriction was examined in healthy pig internal mammary artery (IMA). Tetrodotoxin-, guanethidine-sensitive electrical field stimulation (EFS)-, and noradrenaline-elicited contractions were significantly diminished by prazosin (n=8, P0.001) and less so by rauwolscine, indicating functional α₁- and α₂-adrenoceptor-mediated noradrenergic innervation of the IMA. Endothelium removal reduced neurogenic (n=8, P0.01) but augmented noradrenaline responses (n=8, P0.01), suggesting the release of two endothelium-dependent factors with opposite effects. In the presence of endothelium, neurogenic and…

MaleAdrenergic Antagonistsmedicine.medical_specialtySympathetic Nervous SystemContraction (grammar)EndotheliumArginineSwineBlotting WesternMuscarinic AntagonistsIn Vitro TechniquesNitric OxideBiochemistryNitric oxideNorepinephrinePotassium Channels Calcium-Activatedchemistry.chemical_compoundNerve FibersKATP ChannelsInternal medicinePotassium Channel BlockersPrazosinmedicineAnimalsMammary ArteriesEndothelium-Dependent Relaxing FactorsPharmacologybusiness.industryImmunohistochemistryElectric StimulationPotassium channelmedicine.anatomical_structureEndocrinologychemistryPotassium Channels Voltage-GatedVasoconstrictionProstaglandinsTetrodotoxinEndothelium Vascularmedicine.symptombusinessVasoconstrictionmedicine.drugBiochemical Pharmacology
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Capacitative Ca2+ entry associated with α1-adrenoceptors in rat aorta

1997

In rat aorta, depletion of internal Ca2+ stores by addition of noradrenaline (1 microM) induces a biphasic response (an initial phasic response and a tonic one) mediated by two different intracellular Ca2+ pools. This response cannot be repeated, suggesting a depletion of internal Ca2+ stores sensitive to noradrenaline. In absence of the agonist, this depletion is the signal for the entry of extracellular Ca2+, not only to refill the stores but also, under our experimental conditions, to activate the contractile proteins thus inducing an increase in the resting tone (IRT) that constitutes functional evidence of this Ca2+ entry. The ionic channels involved in the mechanism of the IRT have be…

MaleAgonistCromakalimmedicine.medical_specialtyPotassium Channelsmedicine.drug_classIn Vitro TechniquesTonic (physiology)NorepinephrineReceptors Adrenergic alpha-1medicine.arteryInternal medicineGlyburidePotassium Channel BlockersmedicineExtracellularAnimalsBenzopyransPyrrolesRats WistarCa2 entryAortaIonic ChannelsPharmacologyAortaChemistryGeneral MedicineTetraethylammonium CompoundsCalcium Channel BlockersRatsEndocrinologyMuscle TonusAlpha1 adrenoceptorBiophysicsCalciumNimodipineCalcium ChannelsIntracellularMuscle ContractionNaunyn-Schmiedeberg's Archives of Pharmacology
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Association of a functional deficit of the BKCa channel, a synaptic regulator of neuronal excitability, with autism and mental retardation

2006

International audience; Objective: Autism is a complex, largely genetic psychiatric disorder. In the majority of cases, the cause of autism is not known, but there is strong evidence for a genetic etiology. To identify candidate genes, the physical mapping of balanced chromosomal aberrations is a powerful strategy, since several genes have been characterized in numerous disorders. In this study, the authors analyzed a balanced reciprocal translocation arising de novo in a subject with autism and mental retardation. Method: The authors performed the physical mapping of the balanced 9q23/ 10q22 translocation by fluorescent in situ hybridization experiments using bacterial artificial chromosom…

MaleCandidate geneChromosomes Artificial BacterialIndolesDNA Mutational AnalysisRegulatorChromosomal translocationautism mental retardation KCNMA1 genelarge conductance Ca(2+)-activated K(+) (BK(Ca)) channel synaptic transmission chromosomal translocationSynaptic TransmissionTranslocation GeneticPair 10CA2+-ACTIVATED K+ CHANNELSCloning MolecularChildLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMUTATIONIn Situ HybridizationIn Situ Hybridization FluorescenceReverse Transcriptase Polymerase Chain ReactionBacterialChromosome MappingETIOLOGYPsychiatry and Mental healthArtificialKCNMA1 Gene[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]HaploinsufficiencyPsychologyChromosomes Human Pair 9POTASSIUM CHANNELSHumanPair 9Autistic Disorder; Child; Chromosome Aberrations; Chromosome Mapping; Chromosomes; Artificial; Bacterial; Chromosomes; Human; Pair 10; Chromosomes; Human; Pair 9; Cloning; Molecular; DNA Mutational Analysis; Humans; In Situ Hybridization; Fluorescence; Indoles; Intellectual Disability; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; Male; Reverse Transcriptase Polymerase Chain Reaction; Synaptic Transmission; Translocation; GeneticTranslocationNeurotransmissionChromosomesFluorescenceGeneticIntellectual DisabilitymedicineHumansAutistic DisorderRELEASEChromosome AberrationsCOMPLEXChromosomes Human Pair 10MolecularAutistic Disorder; Child; Chromosome Aberrations; Chromosome Mapping; Chromosomes Artificial Bacterial; Chromosomes Human Pair 10; Chromosomes Human Pair 9; Cloning Molecular; DNA Mutational Analysis; Humans; In Situ Hybridization Fluorescence; Indoles; Intellectual Disability; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; Male; Reverse Transcriptase Polymerase Chain Reaction; Synaptic Transmission; Translocation GeneticPERVASIVE DEVELOPMENTAL DISORDERSmedicine.diseaseDevelopmental disorderINDIVIDUALSLARGE-CONDUCTANCEAutismSCREENNeuroscience[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyCloning
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On the mechanism of action of phenylephrine in rat atrial heart muscle

1994

Both in rat left atrial heart and in aortic smooth muscle preparations, phenylephrine (PE) caused a concentration-dependent increase in force of contraction (FC) in the presence of atenolol (10 mumol/l), which was antagonized by phentolamine, prazosin and WB 4101 in a competitive manner. The pA2 values of the antagonists in the cardiac tissue were 10-20fold lower than those in the rat thoracic aorta. In the spontaneously beating right atrium, PE exerted a positive chronotropic action, which was not significantly antagonized by phentolamine or prazosin. It is therefore assumed that the effects of phenylephrine in the left atrium and in the aorta are mediated by different subtypes of alpha 1-…

MaleChronotropicmedicine.medical_specialtyPotassium ChannelsSodium-Hydrogen ExchangersAction PotentialsIn Vitro TechniquesRats Sprague-DawleyPhenylephrinePhentolamineHeart RateReceptors Adrenergic alpha-1medicine.arteryInternal medicinemedicinePrazosinAnimalsHeart AtriaPhenylephrineAdrenergic alpha-AntagonistsPharmacologyAortaChemistryCalcium RadioisotopesHeartGeneral MedicineAtenololMyocardial ContractionRatsElectrophysiologyActin CytoskeletonEndocrinologyMechanism of actioncardiovascular systemCalciummedicine.symptomAdrenergic alpha-Agonistsmedicine.drugMuscle contractionNaunyn-Schmiedeberg’s Archives of Pharmacology
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Postnatal increases in axonal conduction velocity of an identified Drosophila interneuron require fast sodium, L-type calcium and shaker potassium ch…

2019

Abstract During early postnatal life, speed up of signal propagation through many central and peripheral neurons has been associated with an increase in axon diameter or/and myelination. Especially in unmyelinated axons postnatal adjustments of axonal membrane conductances is potentially a third mechanism but solid evidence is lacking. Here, we show that axonal action potential (AP) conduction velocity in the Drosophila giant fiber (GF) interneuron, which is required for fast long-distance signal conduction through the escape circuit, is increased by 80% during the first day of adult life. Genetic manipulations indicate that this postnatal increase in AP conduction velocity in the unmyelina…

MaleConfirmationaction potential propagationCalcium Channels L-Typepostnatal maturation2Neural ConductionAction PotentialsVoltage-Gated Sodium ChannelsDevelopmentgiant fiberAxonsvoltage-gated ion channels570 Life sciencesnervous systemInterneurons2.6LarvaShaker Superfamily of Potassium ChannelsAnimalsescapeinsectDrosophilaFemale570 Biowissenschaften
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Effects of K(ATP) channel modulators on acetylcholine release from guinea-pig isolated atria and small intestine.

2002

The effects of K(ATP) channel blockers (glibenclamide, HMR 1883, HMR 1372) and openers (cromakalim, pinacidil, diazoxide) on the electrically-evoked (5 Hz) release of [(3)H]acetylcholine were studied in isolated guinea-pig atria and myenteric plexus-longitudinal muscle preparations which had been preincubated with [(3)H]choline. Atria: Cromakalim (0.3 microM and 1 microM), pinacidil (10 microM) and diazoxide (30 microM) significantly reduced the stimulation-evoked release of [(3)H]acetylcholine. The inhibition produced by cromakalim and pinacidil was prevented by 1 microM of either HMR 1883, HMR 1372 or glibenclamide. The blockers alone significantly increased the release at concentrations …

MaleCromakalimPotassium ChannelsGuinea PigsNeuromuscular JunctionMyenteric PlexusPharmacologyIn Vitro Techniqueschemistry.chemical_compoundGlyburideIntestine SmallmedicineDiazoxidePotassium Channel BlockersAnimalsChannel blockerHeart AtriaPharmacologySulfonamidesPinacidilDiazoxideThioureaPotassium channel blockerMuscle SmoothGeneral Medicinemusculoskeletal systemAtrial FunctionMyocardial ContractionHMR 1883Potassium channelAcetylcholinechemistryAnesthesiaPinacidilcardiovascular systemFemaleCromakalimAcetylcholinemedicine.drugNaunyn-Schmiedeberg's archives of pharmacology
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