Birds are an intriguing research object for cardiac physiology: though they, as well as mammalians, developed endothermy and four-chambered high-performance heart, their cardiomyocytes share similar ultrastructure with those in reptilians. Although there are evidences that birds use intracellular Ca2+ stored in SR, Ca2+ cycling and SR Ca2+ storage have not yet been studied in adult avian myocardium. In the present study, we used whole-cell voltage clamp to study sarcolemmal Ca2+ flux, SR Ca2+ storage and the degree of interplay between these sources of Ca2+ in enzymatically isolated cardiomyocytes of Japanese quail (Coturnix japonica). At room temperature, sarcolemmal calcium current (ICa) was present in atrial and ventricular quail cardiomyocytes. In ventricular cells ICa was higher than in atrial myocytes and reached -9.9±1.588 pA/pF at 0 mV (here and further the data presented as mean±s.e.m), which exceeds the reported ICa density in mammalian myocardium (1). According to activation kinetics and the current-voltage curve, I­Ca in adult quail myocardium is presented only by L-type calcium current. We stimulated the cells with 200 ms square pulses applied at 1 Hz frequency to load the SR with Ca2+. SR Ca2+ content was estimated as time-integral of inward current generated by Na+/Ca2+ exchanger activated by application of caffeine. SR Ca2+ accumulation in isolated quail cardiomyocytes was higher than that in mammalian cells (2). In atrial cells the SR content was higher than in ventricular; after 100 pulses it reached 750.6 ± 128.2 μmol l-1 in atrial cells and 423.3 ± 47.2 μmol l-1 in ventricular cells. As Ca2+ was being reaccumulated in SR, sarcolemmal ICa showed calcium-dependent acceleration of inactivation and at room temperature it reached steady-state configuration within 7-10 pulses. It is faster than that in fish cardiomyocytes (3), suggesting tight interaction between LTCC and SR in avian heart. However, we did not observe similar changes in ICa kinetics after depletion of SR Ca2+ stores in quail atrial myocytes. That could resulting from lower ICa amplitude in atrial cells at room temperature or from less favorable distribution of ryanodine receptors in atrial SR. Thus, our study for the first time demonstrates the interaction between large SR Ca2+ stores and LTCC in avian myocardium, which would presumably result in a string gain of Ca2+ signaling during excitation-contraction coupling. Together with considerably large amplitude of sarcolemmal ICa, these mechanisms can provide the high rate and contractility of an avian heart.