Differences in intracellular calcium homeostasis between atrial and ventricular myocytes

The role that Ca2+ plays in ventricular excitation contraction coupling is well defined and much is known about the marked differences in the spatiotemporal properties of the systolic Ca2+ transient between atrial and ventricular myocytes. However, to date there has been no systematic appraisal of the Ca homeostatic mechanisms employed by atrial cells and how these compare to the ventricle. In the present study we sought to determine the fractional contributions made to the systolic Ca2+ transient and the decay of [Ca2+](i) by the sarcoplasmic reticulum and sarcolemmal mechanisms. Experiments were performed on single myocytes isolated from the atria and ventricles of the rat. Intracellular Ca2+ concentration, membrane currents, SR Ca2+ content and cellular Ca2+ buffering capacity were measured at 23 degrees C. Atrial cells had smaller systolic Ca2+ transients (251 +/- 39 vs. 376 +/- 41 nmol.L-1) that decayed more rapidly (7.4 +/- 0.6 vs. 5.45 +/- 0.3 s(-1)). This was due primarily to an increased rate of SR mediated Ca2+ uptake (k(SR), 6.88 +/- 0.6 vs. 4.57 +/- 0.3 s(-1)). SR Ca2+ content was 289% greater and Ca2+ buffering capacity was increased similar to 3-fold in atrial cells (B-max 371.9 +/- 32.4 vs. 121.8 +/- 8 mu mol.L-1, all differences P<0.05). The fractional release of Ca2+ from the SR was greater in atrial cells, although the gain of excitation contraction coupling was the same in both cell types. In summary our data demonstrate fundamental differences in Ca2+ homeostasis between atrial and ventricular cells and we speculate that the increased SIR Ca2+ content may be significant in determining the increased prevalence of arrhythmias in the atria. (C) 2008 Elsevier Inc. All rights reserved.