Effect of Strontium on Transmembrane Potentials of the Rabbit Sino‐Atrial Node Deprived of Calcium

Abstract

HomeCirculation ResearchVol. 28, No. 5Effect of Strontium on Transmembrane Potentials of the Rabbit Sino‐Atrial Node Deprived of Calcium Free AccessResearch ArticlePDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBEffect of Strontium on Transmembrane Potentials of the Rabbit Sino‐Atrial Node Deprived of Calcium NOBORU TODA NOBORU TODANOBORU TODA Department of Pharmacology, Faculty of Medicine, Kyoto University Kyoto, Japan Search for more papers by this author Originally published1 May 1971https://doi.org/10.1161/01.RES.28.5.545Circulation Research. 1971;28:545–553AbstractTransmembrane potentials were recorded from S-A nodal pacemaker and nonpacemaker fibers of the rabbit right atrium. Sr2+ (2.2 mM) prolonged the pacemaker action potentials but did not influence other parameters of the membrane potential. In Ca2+-free solution, maximal diastolic potential, threshold potential, and overshoot were reduced, and the action potential and rise time were prolonged; these changes were enhanced by previous treatment with EGTA (ethyleneglycol bis (β-aminoethylether)-N,N'-tetraacetic acid). In some preparations, pacemaker action potentials disappeared and subthreshold oscillations were observed; Sr2+ and norepinephrine restored action potentials. Addition of Sr2+ to the Ca2+-free solution slowed the pacemaker rate in association with an increase in maximal diastolic potential, threshold potential, overshoot, and action potential duration. In fibers of the right atrium, Sr2+ restored the magnitudes of resting potential and overshoot which had been markedly reduced by zero [Ca2+]o; an ectopic pacemaker was induced. The ability of norepinephrine to induce ectopic automaticity was not increased by Sr2+ at normal [Ca2+]o but was increased at zero [Ca2+]o, Sr2+ partly restored the positive chronotropic effect of sympathetic nerve stimulation which was abolished by removal of Ca2+, but Sr2+ did not correct the reduced susceptibility of the S-A node to exogenous norepinephrine in Ca2+-deficient solutions. It seems likely that Sr2+ can substitute for Ca2+ in maintaining the diastolic membrane potential and overshoot and decreases membrane conductance to K+, which would induce ectopic pacemakers. Previous Back to top Next FiguresReferencesRelatedDetailsCited By Watson B, Woodrough R and March N (1976) The effect of temperature on canine papillary muscle, Biophysics of Structure and Mechanism, 10.1007/BF00863703, 2:2, (99-104), . Refsum H and Landmark K (2009) The Effect of a Calcium-antagonistic Drug, Nifedipine, on the Mechanical and Electrical Activity of the Isolated Rat Atrium, Acta Pharmacologica et Toxicologica, 10.1111/j.1600-0773.1975.tb00855.x, 37:5, (369-376) TODA N (1972) Contractile Responses of Isolated Rabbit Aortae to Transmural Stimulation as Affected by Calcium, Strontium, Sodium and Ouabain, Japanese Journal of Pharmacology, 10.1016/S0021-5198(19)31669-5, 22:3, (347-357), . May 1, 1971Vol 28, Issue 5 Advertisement Article InformationMetrics Copyright copyright 1971 by the American Heart Association, Inc.https://doi.org/10.1161/01.RES.28.5.545 Manuscript receivedDecember 21, 1970Manuscript acceptedMarch 4, 1971Originally publishedMay 1, 1971 Keywordscontractilityright atriumnorepinephrinesympathetic nerve stimulationectopic automaticityPDF download Advertisement