Asynchronous activation of calcium and potassium currents by isoproterenol in canine ventricular myocytes View Full Text


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Article Info

DATE

2014-02-25

AUTHORS

Ferenc Ruzsnavszky, Bence Hegyi, Kornél Kistamás, Krisztina Váczi, Balázs Horváth, Norbert Szentandrássy, Tamás Bányász, Péter P. Nánási, János Magyar

ABSTRACT

Adrenergic activation of L-type Ca2+ and various K+ currents is a crucial mechanism of cardiac adaptation; however, it may carry a substantial proarrhythmic risk as well. The aim of the present work was to study the timing of activation of Ca2+ and K+ currents in isolated canine ventricular cells in response to exposure to isoproterenol (ISO). Whole cell configuration of the patch-clamp technique in either conventional voltage clamp or action potential voltage clamp modes were used to monitor ICa, IKs, and IKr, while action potentials were recorded using sharp microelectrodes. ISO (10 nM) elevated the plateau potential and shortened action potential duration (APD) in subepicardial and mid-myocardial cells, which effects were associated with multifold enhancement of ICa and IKs and moderate stimulation of IKr. The ISO-induced plateau shift and ICa increase developed faster than the shortening of APD and stimulation of IKs and IKr. Blockade of β1-adrenoceptors (using 300 nM CGP-20712A) converted the ISO-induced shortening of APD to lengthening, decreased its latency, and reduced the plateau shift. In contrast, blockade of β2-adrenoceptors (by 50 nM ICI 118,551) augmented the APD-shortening effect and increased the latency of plateau shift without altering its magnitude. All effects of ISO were prevented by simultaneous blockade of both receptor types. Inhibition of phosphodiesterases decreased the differences observed in the turn on of the ISO-induced plateau shift and APD shortening. ISO-induced activation of ICa is turned on faster than the stimulation of IKs and IKr in canine ventricular cells due to the involvement of different adrenergic pathways and compartmentalization. More... »

PAGES

457-467

References to SciGraph publications

  • 1993-08. A comparative analysis of the time course of cardiac Ca2+ current response to rapid applications of β-adrenergic and dihydropyridine agonists in NAUNYN-SCHMIEDEBERG'S ARCHIVES OF PHARMACOLOGY
  • 1987-04. β2-Adrenoceptor-mediated positive inotropic effect of adrenaline in human ventricular myocardium in NAUNYN-SCHMIEDEBERG'S ARCHIVES OF PHARMACOLOGY
  • 1988-02. β-Adrenergic modulation in the heart in PFLÜGERS ARCHIV - EUROPEAN JOURNAL OF PHYSIOLOGY
  • 2010-07-29. Effects of ropinirole on action potential characteristics and the underlying ion currents in canine ventricular myocytes in NAUNYN-SCHMIEDEBERG'S ARCHIVES OF PHARMACOLOGY
  • 2005-06-11. Asymmetrical distribution of ion channels in canine and human left-ventricular wall: epicardium versus midmyocardium in PFLÜGERS ARCHIV - EUROPEAN JOURNAL OF PHYSIOLOGY
  • 2012-12-15. Sex differences in repolarization and slow delayed rectifier potassium current and their regulation by sympathetic stimulation in rabbits in PFLÜGERS ARCHIV - EUROPEAN JOURNAL OF PHYSIOLOGY
  • 1985-10. Direct labelling of β2-adrenoceptors in NAUNYN-SCHMIEDEBERG'S ARCHIVES OF PHARMACOLOGY
  • 2012-12-19. Effects of tacrolimus on action potential configuration and transmembrane ion currents in canine ventricular cells in NAUNYN-SCHMIEDEBERG'S ARCHIVES OF PHARMACOLOGY
  • 1990-05. Ionic currents contributing to the action potential in single ventricular myocytes of the guinea pig studied with action potential clamp in PFLÜGERS ARCHIV - EUROPEAN JOURNAL OF PHYSIOLOGY
  • 2008-07-05. Contribution of IKr and IK1 to ventricular repolarization in canine and human myocytes: is there any influence of action potential duration? in BASIC RESEARCH IN CARDIOLOGY
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s00210-014-0964-6

    DOI

    http://dx.doi.org/10.1007/s00210-014-0964-6

    DIMENSIONS

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    PUBMED

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    27 schema:description Adrenergic activation of L-type Ca2+ and various K+ currents is a crucial mechanism of cardiac adaptation; however, it may carry a substantial proarrhythmic risk as well. The aim of the present work was to study the timing of activation of Ca2+ and K+ currents in isolated canine ventricular cells in response to exposure to isoproterenol (ISO). Whole cell configuration of the patch-clamp technique in either conventional voltage clamp or action potential voltage clamp modes were used to monitor ICa, IKs, and IKr, while action potentials were recorded using sharp microelectrodes. ISO (10 nM) elevated the plateau potential and shortened action potential duration (APD) in subepicardial and mid-myocardial cells, which effects were associated with multifold enhancement of ICa and IKs and moderate stimulation of IKr. The ISO-induced plateau shift and ICa increase developed faster than the shortening of APD and stimulation of IKs and IKr. Blockade of β1-adrenoceptors (using 300 nM CGP-20712A) converted the ISO-induced shortening of APD to lengthening, decreased its latency, and reduced the plateau shift. In contrast, blockade of β2-adrenoceptors (by 50 nM ICI 118,551) augmented the APD-shortening effect and increased the latency of plateau shift without altering its magnitude. All effects of ISO were prevented by simultaneous blockade of both receptor types. Inhibition of phosphodiesterases decreased the differences observed in the turn on of the ISO-induced plateau shift and APD shortening. ISO-induced activation of ICa is turned on faster than the stimulation of IKs and IKr in canine ventricular cells due to the involvement of different adrenergic pathways and compartmentalization.
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