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

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 Ca 2+ 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 Ca 2+ 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 Ca 2+ release from the sarcoplasmic reticulum, has little impact on steady-state tension generation. This would suggest that myofilament Ca 2+ 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 Ca 2+ 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 Ca 2+ efflux is determined by two SL proteins: Na + –Ca 2+ exchange and the Ca 2+ pump. However, there may be conditions in the hearts of active teleosts in which SR Ca 2+ release is of physiological consequence. The contribution of these transport systems to the delivery and removal of Ca 2+ from the myofilaments with each beat is discussed.