Cholinergic-adrenergic Antagonism In The Induction Of Tachyarrhythmia By Electrical Stimulation In Isolated Rat Atria.

dc.creatorZafalon, Nivaldo
dc.creatorBassani, José W M
dc.creatorBassani, Rosana A
dc.date2004-Jul
dc.date2015-11-27T12:58:17Z
dc.date2015-11-27T12:58:17Z
dc.date.accessioned2018-03-29T00:59:16Z
dc.date.available2018-03-29T00:59:16Z
dc.identifierJournal Of Molecular And Cellular Cardiology. v. 37, n. 1, p. 127-35, 2004-Jul.
dc.identifier0022-2828
dc.identifier10.1016/j.yjmcc.2004.04.020
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/15242743
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/195859
dc.identifier15242743
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1296092
dc.descriptionAtrial tachyarrhythmias (AT) are the most common cardiac rhythm disturbance. In the present study, we analyzed the cholinergic-adrenergic interaction in the in vitro induction of cholinergic-dependent tachyarrhythmia by high-frequency electric stimulation. Tachyarrhythmia was evoked in isolated rat right atria by trains of electric stimuli. Atrial response was expressed as the tachyarrhythmia induction index (ATI, i.e. the fraction of applied trains that resulted in arrhythmia induction). ATI was reversibly increased by 0.6 microM carbachol (CCh), which also decreased atrial spontaneous rate (ASR). In contrast, 10 nM isoproterenol (ISO), 100 microM tyramine and the phosphodiesterase inhibitor isobutyl-methylxanthine (IBMX, 100 microM) increased ASR and decreased ATI. Amiodarone (AMI, 10 microM) reduced ATI in the presence and absence of CCh. Further CCh addition restored ATI in atria treated with either IBMX or AMI, but not when both compounds were present. Increase in ATI by CCh in atria pretreated with IBMX plus ISO was significantly attenuated by 3 mM NaF. The antagonism between cholinergic muscarinic and beta-adrenergic receptor stimulation (the former facilitating and the latter inhibiting tachyarrhythmia installation) possibly involves regulation of the phosphorylation status of adenosine cyclic 3'-5'-monophosphate (cAMP)-dependent protein kinase substrates. Additionally, cAMP-independent, AMI-sensitive mechanism stimulated by CCh (possibly muscarinic-dependent K(+) current activation) seems to contribute to AT facilitation.
dc.description37
dc.description127-35
dc.languageeng
dc.relationJournal Of Molecular And Cellular Cardiology
dc.relationJ. Mol. Cell. Cardiol.
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subject1-methyl-3-isobutylxanthine
dc.subjectAmiodarone
dc.subjectAnimals
dc.subjectAnti-arrhythmia Agents
dc.subjectCarbachol
dc.subjectCholinergic Agonists
dc.subjectCyclic Amp
dc.subjectDisease Models, Animal
dc.subjectDose-response Relationship, Drug
dc.subjectElectric Stimulation
dc.subjectElectrophysiology
dc.subjectHeart Atria
dc.subjectMale
dc.subjectPhosphodiesterase Inhibitors
dc.subjectPhosphoric Monoester Hydrolases
dc.subjectPhosphorylation
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectReceptors, Adrenergic
dc.subjectReceptors, Cholinergic
dc.subjectReceptors, Muscarinic
dc.subjectSodium Fluoride
dc.subjectTachycardia
dc.subjectTime Factors
dc.titleCholinergic-adrenergic Antagonism In The Induction Of Tachyarrhythmia By Electrical Stimulation In Isolated Rat Atria.
dc.typeArtículos de revistas


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