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

Abstract

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 resemble 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 transsarcolemmal and intracellular Ca2+ channel interplay in freshly isolated atrial and ventricular myocytes from the heart of the Japanese quail (Coturnix japonica). A transsarcolemmal Ca2+ current was detectable both in quail atrial and ventricular myocytes and was mediated only by L-type Ca2+ channels. The peak density of ICa was larger in ventricular cells than in atrial 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 24⁰C. We observed SR-Ca2+-dependent inactivation of ICa 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.