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Cardiovascular Research 2001 52(1):76-83; doi:10.1016/S0008-6363(01)00363-7
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

On the source of Ca2+ activating the tonic component of contraction of myocytes of guinea pig heart

Krzysztof Emanuel, Urszula Mackiewicz and Bohdan Lewartowski*

Department of Clinical Physiology, Medical Centre of Postgraduate Education, Marymoncka 99, 01-813 Warsaw, Poland

blew{at}cmkp.edu

* Corresponding author. Tel.: +48-22-834-0367; fax: +48-22-864-0834

Objective: Contractions of isolated, single myocytes of guinea pig heart stimulated at 37°C consist of a phasic component and a voltage dependent tonic component. In this study we investigated the source of Ca2+ activating the tonic component. Methods: Experiments were performed at 37°C in ventricular myocytes of guinea pig heart. Voltage-clamped cells were stimulated by the pulses from the holding potential of –40 to +5 mV. [Ca2+]i was monitored as fluorescence of Indo 1-AM and contractions were recorded with the TV edge-tracking system. Results: Superfusion of 5 mmol/l Ni2+ during 30 s pause did not inhibit subsequent biphasic Ca2+ transients and contractions despite inhibition of Ca2+ current and Na+/Ca2+ exchange. KB-R7943 (5 µmol/l) or intracellular dialysis with 0 Na+ solution, both of which inhibit reversed Na+/Ca2+ exchange, decreased amplitude of Ca2+ transients and contractions by ~40%. The ratio of amplitudes of tonic to phasic component was increased by Ni2+ and was not changed by KB-R7943 or 0 Na+i. Ryanodine (200 µmol/l) inhibited both components of contractions in cells superfused with Ni2+. The phasic component but not the tonic component was inhibited by 20 µmol/l nifedipine in cells superfused with Ni2+. Conclusions: Tonic component of contraction of single myocytes of guinea pig heart is not activated by Ca2+ current or by the reverse mode Na+/Ca2+ exchange as currently proposed in literature. Rather, it is activated by Ca2+ released from the sarcoplasmic reticulum. However, kinetics and mechanism of release seem to be quite different from those of Ca2+ fraction activating the phasic component of contraction.

KEYWORDS Myocytes; Contractile function; e–c Coupling; Calcium (cellular)


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