Warmer, faster, stronger: Ca²⁺ cycling in avian myocardium

Birds occupy a unique position in the evolution of cardiac design. Their hearts are capable of cardiac performance on par with, or exceeding that of mammals, and yet the structure of their cardiomyocytes resembles those of reptiles. It has been suggested that birds use intracellular Ca²⁺ stored within the sarcoplasmic reticulum (SR) to power contractile function, but neither SR Ca²⁺ content nor the cross-talk between channels underlying Ca²⁺-induced Ca²⁺ release (CICR) have been studied in adult birds. Here we used voltage clamp to investigate the Ca²⁺ storage and refilling capacities of the SR and the degree of trans-sarcolemmal and intracellular Ca²⁺ channel interplay in freshly isolated atrial and ventricular myocytes from the heart of the Japanese quail (Coturnix japonica). A trans-sarcolemmal Ca²⁺ current (I_Ca) was detectable in both quail atrial and ventricular myocytes, and was mediated only by L-type Ca²⁺ channels. The peak density of I_Ca was larger in ventricular cells than in atrial cells, and exceeded that reported for mammalian myocardium recorded under similar conditions. Steady-state SR Ca²⁺ content of quail myocardium was also larger than that reported for mammals, and reached 750.6±128.2 μmol l^-1 in atrial cells and 423.3±47.2 μmol l^-1 in ventricular cells at 24°C. We observed SR Ca²⁺-dependent inactivation of I_Ca in ventricular myocytes, indicating cross-talk between sarcolemmal Ca²⁺ channels and ryanodine receptors in the SR. However, this phenomenon was not observed in atrial myocytes. Taken together, these findings help to explain the high-efficiency avian myocyte excitation-contraction coupling with regard to their reptilian-like cellular ultrastructure.