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 Ca²⁺ 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 °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 ∼3-fold in atrial cells (B_max 371.9±32.4 vs. 121.8±8 μmol.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 SR Ca²⁺ content may be significant in determining the increased prevalence of arrhythmias in the atria.