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- Title
Diversity of atrial local Ca<sup>2+</sup> signalling: evidence from 2-D confocal imaging in Ca<sup>2+</sup>-buffered rat atrial myocytes.
- Authors
Sun-Hee Woo; Cleemann, Lars; Morad, Martin
- Abstract
Atrial myocytes, lacking t-tubules, have two functionally separate groups of ryanodine receptors (RyRs): those at the periphery colocalized with dihydropyridine receptors (DHPRs), and those at the cell interior not associated with DHPRs. We have previously shown that the Ca2+ current ( ICa)-gated central Ca2+ release has a fast component that is followed by a slower and delayed rising phase. The mechanisms that regulate the central Ca2+ releases remain poorly understood. The fast central release component is highly resistant to dialysed Ca2+ buffers, while the slower, delayed component is completely suppressed by such exogenous buffers. Here we used dialysis of Ca2+ buffers (EGTA) into voltage-clamped rat atrial myocytes to isolate the fast component of central Ca2+ release and examine its properties using rapid (240 Hz) two-dimensional confocal Ca2+ imaging. We found two populations of rat atrial myocytes with respect to the ratio of central to peripheral Ca2+ release ( Rc/p). In one population (‘group 1’, ∼60% of cells), Rc/p converged on 0.2, while in another population (‘group 2’, ∼40%), Rc/p had a Gaussian distribution with a mean value of 0.625. The fast central release component of group 2 cells appeared to result from in-focus Ca2+ sparks on activation of ICa. In group 1 cells intracellular membranes associated with t-tubular structures were never seen using short exposures to membrane dyes. In most of the group 2 cells, a faint intracellular membrane staining was observed. Quantification of caffeine-releasable Ca2+ pools consistently showed larger central Ca2+ stores in group 2 and larger peripheral stores in group 1 cells. The Rc/p was larger at more positive and negative voltages in group 1 cells. In contrast, in group 2 cells, the Rc/p was constant at all voltages. In group 1 cells the gain of peripheral Ca2+ release sites (Δ[Ca2+]/ ICa) was larger at −30 than at +20 mV, but significantly dampened at the central sites. On the other hand, the gains of peripheral and central Ca2+ releases in group 2 cells showed no voltage dependence. Surprisingly, the voltage dependence of the fast central release component was bell-shaped and similar to that of ICa in both cell groups. Removal of extracellular Ca2+ or application of Ni2+ (5 m m) suppressed equally ICa and Ca2+ release from the central release sites at +60 mV. Depolarization to +100 mV, where ICa is absent and the Na+–Ca2+ exchanger (NCX) acts in reverse mode, did not trigger the fast central Ca2+ releases in either group, but brief reduction of [Na+]o to levels equivalent to [Na+]i facilitated fast peripheral and central Ca2+ releases in group 2 myocytes, but not in group 1 myocytes. In group 2 cells, long-lasting (> 1 min) exposures to caffeine (10 m m) or ryanodine (20 μ m) significantly suppressed ICa-triggered central and peripheral Ca2+ releases. Our data suggest significant diversity of local Ca2+ signalling in rat atrial myocytes. In one group, ICa-triggered peripheral Ca2+ release propagates into the interior triggering central Ca2+ release with significant delay. In a second group of myocytes ICa triggers a significant number of central sites as rapidly and effectively as the peripheral sites, thereby producing more synchronized Ca2+ releases throughout the myocytes. The possible presence of vestigial t-tubules and larger Ca2+ content of central sarcoplasmic reticulum (SR) in group 2 cells may be responsible for the rapid and strong activation of central release of Ca2+ in this subset of atrial myocytes.
- Publication
Journal of Physiology, 2005, Vol 567, Issue 3, p905
- ISSN
0022-3751
- Publication type
Academic Journal
- DOI
10.1113/jphysiol.2005.092270