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 (I_Ca)‐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 (R_c/p). In one population (‘group 1’, ∼60% of cells), R_c/p converged on 0.2, while in another population (‘group 2’, ∼40%), R_c/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 I_Ca. 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 R_c/p was larger at more positive and negative voltages in group 1 cells. In contrast, in group 2 cells, the R_c/p was constant at all voltages. In group 1 cells the gain of peripheral Ca²⁺ release sites (Δ[Ca²⁺]/I_Ca) 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 I_Ca in both cell groups. Removal of extracellular Ca²⁺ or application of Ni²⁺ (5 mm) suppressed equally I_Ca and Ca²⁺ release from the central release sites at +60 mV. Depolarization to +100 mV, where I_Ca 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 mm) or ryanodine (20 μm) significantly suppressed I_Ca‐triggered central and peripheral Ca²⁺ releases. Our data suggest significant diversity of local Ca²⁺ signalling in rat atrial myocytes. In one group, I_Ca‐triggered peripheral Ca²⁺ release propagates into the interior triggering central Ca²⁺ release with significant delay. In a second group of myocytes I_Ca 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.