Calcium transport and the regulation of cardiac contractility in teleosts: a comparison with higher vertebrates

Abstract

Active teleosts such as the salmonids must vary cardiac output severalfold over a wide range of temperatures. Myocardial contractility, an important determinant of cardiac output, must be maintained and regulated in these species under conditions that are cardioplegic to mammals. Contractility is determined primarily by the magnitude and rate of calcium delivery to the myofilaments. In mammals, a relatively small Ca2+ influx across the sarcolemma (SL) triggers the release of a larger pool of calcium from the sarcoplasmic reticulum (SR). In teleosts and other lower vertebrates, release of Ca2+ from the sarcoplasmic reticulum appears to be less important than in mammals, based primarily on the following findings: (i) electron micrographs of the ventricles of these species indicate that the sarcoplasmic reticulum is relatively sparse, and (ii) ryanodine, an alkaloid that blocks Ca2+ release from the sarcoplasmic reticulum, has little impact on steady-state tension generation. This would suggest that myofilament Ca2+ delivery is controlled primarily by calcium influx across the sarcolemma, which presumably occurs through the voltage-dependent L-type calcium channel. In the absence of a prominent role for Ca2+ release from the sarcoplasmic reticulum under most physiological conditions, therefore, it follows that that the rate of mechanical relaxation is determined primarily by the rate of efflux of calcium across the sarcolemma. The trans-sarcolemmal Ca2+ efflux is determined by two SL proteins: Na+–Ca2+ exchange and the Ca2+ pump. However, there may be conditions in the hearts of active teleosts in which SR Ca2+ release is of physiological consequence. The contribution of these transport systems to the delivery and removal of Ca2+ from the myofilaments with each beat is discussed.