| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on August 16, 2002
Revised on November 27, 2002
Accepted on December 2, 2002
From the Department of Pharmacology, Georgetown University Medical Center, Washington, DC.
* To whom correspondence should be addressed. E-mail: moradm{at}georgetown.edu.
Atrial myocytes have two functionally separate Ca2+ release sites: those in peripheral sarcoplasmic reticulum (SR) adjacent to the Ca2+ channels of surface membrane and those in central SR not associated with Ca2+ channels. Recently, we have reported on the gating of these two different Ca2+ release sites by Ca2+ current. In the present study, we report on the spatiotemporal properties of focal Ca2+ releases (sparks) occurring spontaneously in central and peripheral sites of voltage-clamped rat atrial myocytes, using rapid 2-dimensional (2-D) confocal Ca2+ imaging. Peripheral and central sparks were similar in size and release time (
300 000 Ca2+ ions for
12 ms), but significantly larger and longer than ventricular sparks. Both sites were resistant to Cd2+ and inhibited by ryanodine. Peripheral sparks were brighter and flattened against surface membrane, had
5-fold higher frequency,
2 times faster diffusion coefficient, and dissipated abruptly. Central sparks, in contrast, occurred less frequently, were elongated along the cellular longitudinal axis, and dissipated slowly. Compound sparks (composed of 2 to 5 unitary focal releases) aligned longitudinally and occurred more frequently at the center. The diversity of peripheral and central sparks with respect to shape, frequency, and speed of spatial development and decay is consistent with regional ultrastructural heterogeneity of SR. The retarded dissipation of central atrial sparks, and high prevalence of compound sparks in cell center may be critical in facilitating the propagation of Ca2+ waves in atrial myocytes lacking t tubular system and provide the atrial myocytes with functional Ca2+ signaling diversity.
This article has been cited by other articles:
![]() |
P. Sasse, J. Zhang, L. Cleemann, M. Morad, J. Hescheler, and B. K. Fleischmann Intracellular Ca2+ Oscillations, a Potential Pacemaking Mechanism in Early Embryonic Heart Cells J. Gen. Physiol., July 30, 2007; 130(2): 133 - 144. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. E. D. J. ter Keurs and P. A. Boyden Calcium and Arrhythmogenesis Physiol Rev, April 1, 2007; 87(2): 457 - 506. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Hatem Does the loss of transverse tubules contribute to dyssynchronous Ca2+ release during heart failure? Cardiovasc Res, April 1, 2004; 62(1): 1 - 3. [Full Text] [PDF] |
||||
|
Circulation Research Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2002 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |