We have characterized the dependence on membrane potential (V_m) and calcium current (I_Ca) of calcium‐induced calcium release (CICR) from the junctional‐SR (j‐SR, in the subsarcolemmal (SS) space) and non‐junctional‐SR (nj‐SR, in the central (CT) region of the cell) of cat atrial myocytes using whole‐cell voltage‐clamp together with spatially resolved laser‐scanning confocal microscopy. Subsarcolemmal and central [Ca²⁺]_i transient amplitudes and I_Ca had a bell‐shaped dependence on V_m, but [Ca²⁺]_i reached a maximum at more negative V_m (‐10 to 0 mV) than I_Ca (+10 mV). Termination of I_Ca after a brief depolarization (2.5 to 22.5 ms) immediately interrupted only the SS [Ca²⁺]_i transient, leaving the development of the CT [Ca²⁺]_i transient unaffected. Block of SR function with 20 μm ryanodine and 2 μm thapsigargin, revealed that > 90 % of the control [Ca²⁺]_i transient amplitude was attributable to active SR Ca²⁺ release through ryanodine receptors (RyRs). The gain of SR Ca²⁺ release was highest in the SS space at negative test potentials and was less pronounced in the CT region. Inhibition of Na⁺‐Ca²⁺ exchange resulted in prolonged and higher amplitude [Ca²⁺]_i transients, elevated resting [Ca²⁺]_i, accelerated propagation of CICR, decreased extrusion of Ca²⁺ and an increase in j‐SR Ca²⁺ load. Increasing the cytosolic Ca²⁺ buffer capacity by internal perfusion with 1 mm EGTA limited SR Ca²⁺ release to the SS region, indicating that Ca²⁺ release from nj‐SR is initiated by diffusion of Ca²⁺ from the cell periphery and propagating CICR. Junctional‐SR Ca²⁺ release occurred at discrete sites whose order of activation and amplitude of release varied from beat to beat. In conclusion, during normal excitation‐contraction coupling in cat atrial myocytes, only Ca²⁺ release from the j‐SR is directly activated by Ca²⁺ entering via I_Ca. Elevation of SS [Ca²⁺]_i is required to provide the cytosolic Ca²⁺ gradient needed to initiate regenerative and propagating CICR from nj‐SR.