Diastolic SR Ca efflux in atrial pacemaker cells and Ca-overloaded myocytes

dc.creatorBassani, RA
dc.creatorBassani, JWM
dc.creatorLipsius, SL
dc.creatorBers, DM
dc.date1997
dc.dateAUG
dc.date2014-07-30T14:42:22Z
dc.date2015-11-26T16:43:53Z
dc.date2014-07-30T14:42:22Z
dc.date2015-11-26T16:43:53Z
dc.date.accessioned2018-03-28T23:29:02Z
dc.date.available2018-03-28T23:29:02Z
dc.identifierAmerican Journal Of Physiology-heart And Circulatory Physiology. Amer Physiological Soc, v. 273, n. 2, n. H886, n. H892, 1997.
dc.identifier0363-6135
dc.identifierWOS:A1997XQ29500044
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/61701
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/61701
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1273731
dc.descriptionEvidence has shown that the sarcoplasmic reticulum (SR) of cardiac cells releases Ca not only during excitation-contraction coupling but also during diastole, albeit at a much lower rate. This diastolic SR Ca release (leak) has also been implicated in the generation of spontaneous depolarization in latent atrial pacemaker cells of the cat right atrium. In the present work, we sought to measure Ca transients in pacemaker and nonpacemaker cells of the cat using the fluorescent Ca indicator indo 1. Atrial latent pacemaker cells develop a slow Ca transient when rested in the presence of both Na- and Ca-free solution and thapsigargin [used to inhibit Na/Ca exchange and SR Ca adenosinetriphosphatase (Ca-ATPase), respectively]. This increase in cytosolic Ca concentration ([Ca](i)) is probably caused by the rate of SR Ca leak exceeding the capacity of the remaining Ca transport systems (e.g., sarcolemmal Ca-ATPase and mitochondrial Ca uptake). However, neither cat sinoatrial (SA) node cells nor myocytes from cat atrium or ventricle exhibited a similar increase in [Ca](i) during the same protocol. This indicates that SR Ca leak in these cells occurred at a rate low enough to be within the capacity of the slow Ca transporters, as observed previously in rabbit ventricular myocytes. When atrial and ventricular myocytes were stimulated at higher frequencies, sufficient to markedly increase diastolic and systolic [Ca](i) and approach Ca overload (and spontaneous activity), they responded to inhibition of SR Ca-ATPase and Na/Ca exchange with a slow Ca transient similar to that normally observed in atrial latent pacemaker cells. Furthermore, the SR Ca depletion by thapsigargin did not affect spontaneous activity of SA node cells, but it prevented or slowed pacemaker activity in the atrial latent pacemaker cells. These findings suggest that enhanced diastolic SR Ca efflux contributes significantly to the generation of spontaneous activity in atrial subsidiary pacemakers under normal conditions and in Ca-overloaded myocytes but not in SA node cells.
dc.descriptiono TEXTO COMPLETO DESTE ARTIGO, ESTARÁ DISPONÍVEL À PARTIR DE AGOSTO DE 2015.
dc.description273
dc.description2
dc.descriptionH886
dc.descriptionH892
dc.languageen
dc.publisherAmer Physiological Soc
dc.publisherBethesda
dc.relationAmerican Journal Of Physiology-heart And Circulatory Physiology
dc.relationAm. J. Physiol.-Heart Circul. Physiol.
dc.rightsembargo
dc.sourceWeb of Science
dc.subjectsinoatrial node cells
dc.subjectsarcoplasmic reticulum calcium release
dc.subjectthapsigargin
dc.subjectcalcium transients
dc.subjectautomaticity
dc.subjectRat Ventricular Myocytes
dc.subjectSarcoplasmic-reticulum
dc.subjectCardiac-muscle
dc.subjectRabbit
dc.subjectCalcium
dc.subjectRelease
dc.subjectPotentiation
dc.subjectRelaxation
dc.subjectMechanisms
dc.subjectExchange
dc.titleDiastolic SR Ca efflux in atrial pacemaker cells and Ca-overloaded myocytes
dc.typeArtículos de revistas


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