Differences in intracellular calcium homeostasis between atrial and ventricular myocytes.

The role that Ca(2+) plays in ventricular excitation contraction coupling is well defined and much is known about the marked differences in the spatiotemporal properties of the systolic Ca(2+) transient between atrial and ventricular myocytes. However, to date there has been no systematic appraisal of the Ca(2+) 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 Ca(2+) transient and the decay of [Ca(2+)](i) by the sarcoplasmic reticulum and sarcolemmal mechanisms. Experiments were performed on single myocytes isolated from the atria and ventricles of the rat. Intracellular Ca(2+) concentration, membrane currents, SR Ca(2+) content and cellular Ca(2+) buffering capacity were measured at 23 degrees C. Atrial cells had smaller systolic Ca(2+) transients (251+/-39 vs. 376+/-41 nmol x 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 Ca(2+) uptake (k(SR), 6.88+/-0.6 vs. 4.57+/-0.3 s(-1)). SR Ca(2+) content was 289% greater and Ca(2+) buffering capacity was increased approximately 3-fold in atrial cells (B(max) 371.9+/-32.4 vs. 121.8+/-8 micromol x L(-1), all differences P<0.05). The fractional release of Ca(2+) 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 Ca(2+) homeostasis between atrial and ventricular cells and we speculate that the increased SR Ca(2+) content may be significant in determining the increased prevalence of arrhythmias in the atria.