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First published online on May 24, 2002.
 Copyright © 2002 by The Physiological Society
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2001.013382v1
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Received October 9, 2001
Accepted after revision April 30, 2002

Spatial characteristics of sarcoplasmic reticulum Ca2+ release events triggered by L-type Ca2+ current and Na+ current in guinea-pig cardiac myocytes

P. Lipp1*, Marcel Egger2, and Ernst Niggli2

1 Institute for Molecular Cell Biology, University of the Saarland, Building 61, 66421 Homburg/Saar, Germany
2 Department of Physiology, University of Bern, Bühlplatz 5, 3012 Bern, Switzerland

* To whom correspondence should be addressed. E-mail: peter.lipp{at}uniklinik-saarland.de.

Ca2+ signals in cardiac muscle cells are composed of spatially limited elementary events termed Ca2+ sparks. Several studies have also indicated that Ca2+ signals smaller than Ca2+ sparks can be elicited. These signals have been termed Ca2+ quarks and were proposed to result from the opening of a single Ca2+ release channel of the sarcoplasmic reticulum. We used laser-scanning confocal microscopy to examine the subcellular properties of Na+ current (INa)- and L-type Ca2+ current (ICa,L)-induced Ca2+ transients in voltage-clamped ventricular myocytes isolated from guinea-pigs. Both currents, INa and ICa,L, evoked substantial, global Ca2+ transients. To examine the spatiotemporal properties of such Ca2+ signals, we performed power spectral analysis of these Ca2+ transients and found that both lacked spatial frequency components characteristic for Ca2+ sparks. The application of 10 µM verapamil to partially block L-type Ca2+ current reduced the corresponding Ca2+ transients down to individual Ca2+ sparks. In contrast, INa-induced Ca2+ responses were still spatially homogeneous and lacked Ca2+ sparks even for small current amplitudes. By using high resistance patch pipettes (> 4 M{Omega}) to exaggerate the loss of voltage control during INa, Ca2+ sparks appeared superimposed on a homogeneous Ca2+ release component and were exclusively triggered during the flow of INa. In the presence of 10 µM ryanodine both ICa,L and INa elicited small, residual Ca2+ transients that were spatially homogeneous but displayed distinctively different temporal profiles. We conclude that INa is indeed able to cause Ca2+ release in guinea-pig ventricular myocytes. In contrast to ICa,L-induced Ca2+ transients, which are built up from the recruitment of individual Ca2+ sparks, the INa-evoked cellular responses were always homogeneous, indicating that their underlying elementary Ca2+ release event is distinct from the Ca2+ spark. Thus, INa-induced Ca2+ transients are composed of smaller Ca2+ signals, most likely Ca2+ quarks.




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