Triggering of sarcoplasmic reticulum Ca2+ release and contraction by reverse mode Na+/Ca2+ exchange in trout atrial myocytes

Leif Hove-Madsen, Anna Llach, Glen F. Tibbits, Lluis Tort

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    28 Citations (Scopus)


    Whole cell patch clamp and intracellular Ca2+ transients in trout atrial cardiomyocytes were used to quantify calcium release from the sarcoplasmic reticulum (SR) and examine its dependency on the Ca2+ trigger source. Short depolarization pulses (2-20 ms) elicited large caffeine-sensitive tail currents. The Ca2+ carried by the caffeine-sensitive tail current after a 2-ms depolarization was 0.56 amol Ca2+/pF, giving an SR Ca2+ release rate of 279 amol Ca2+·pF-1·s-1 or 4.3 mM/s. Depolarizing cells for 10 ms to different membrane potentials resulted in a local maximum of SR Ca2+ release, intracellular Ca2+ transient, and cell shortening at 10 mV. Although 100 μM CdCl2 abolished this local maximum, it had no effect on SR Ca2+ release elicited by a depolarization to 110 or 150 mV, and the SR Ca2+ release was proportional to the membrane potential in the range -50 to 150 mV with 100 μM CdCl2. Increasing the intracellular Na+ concentration ([Na+]) from 10 to 16 mM enhanced SR Ca2+ release but reduced cell shortening at all membrane potentials examined. In the absence of TTX, SR Ca2+ release was potentiated with 16 mM but not 10 mM pipette [Na+]. Comparison of the total sarcolemmal Ca2+ entry and the Ca2+ released from the SR gave a gain factor of 18.6 ± 7.7. Nifedipine (Nif) at 10 μM inhibited L-type Ca2+ current (ICa) and reduced the time integral of the tail current by 61%. The gain of the Nif-sensitive SR Ca2+ release was 16.0 ± 4.7. A 2-ms depolarization still elicited a contraction in the presence of Nif that was abolished by addition of 10 mM NiCl2. The gain of the Nifinsensitive but NiCl2-sensitive SR Ca2+ release was 14.8 ± 7.1. Thus both reverse-mode Na+/Ca2+ exchange (NCX) and ICa can elicit Ca2+ release from the SR, but ICa is more efficient than reverse-mode NCX in activating contraction. This difference may be due to extrusion of a larger fraction of the Ca2+ released from the SR by reverse-mode NCX rather than a smaller gain for NCX-induced Ca2+ release.
    Original languageEnglish
    JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
    Issue number5 53-5
    Publication statusPublished - 1 May 2003


    • Ca current 2+
    • Ca transients 2+
    • Caffeine
    • Cardiac
    • Excitation-contraction coupling


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