The Cardiac Na⁺‐Ca²⁺Exchanger

Sex differences in expression of calcium-handling proteins and beta-adrenergic receptors in rat heart ventricle

“…Interestingly, Tadros et al (Tadros et al, 2002) showed that transfection of rat cardiomyocytes with antisense oligonucleotides to NCX resulted in delayed relaxation after caffeine-induced contracture (in the absence of changes in other Ca 2+ -handling proteins), but overall contractile activity in these cells was not significantly altered in the presence of physiological levels of extracellular Ca 2+ . In other studies of transgenic mouse cardiomyocytes, rates of contraction and relaxation have been found to increase but the effect is often small and the results of studies vary (Cross et al, 1998;Hryshko, 2002).…”

Changes in extracellular K+ concentration modulate contractility of rat and rabbit cardiac myocytes via the inward rectifier K+ current IK1

“…The sarcolemmal Na + -Ca 2+ exchanger is known to be the major mechanism responsible for removing Ca 2+ from cardiac cells (Hryshko, 2002;Bers et al 2003). We have shown previously (Bouchard et al 1993a) that hyperpolarization of diastolic potential results in a marked negative inotropic effect in rat ventricular myocytes.…”

“…Elevation of [Ca 2+ ] i during a Ca 2+ transient is a function of Ca 2+ influx through voltage-gated Ca 2+ channels, which in turn triggers Ca 2+ release from SR stores via CICR. While it is possible that under some conditions Ca 2+ influx through the sarcolemmal Na + -Ca 2+ exchanger can increase [Ca 2+ ] i (Baczko et al 2003), the main function of the exchanger under physiological conditions is to extrude Ca 2+ from the cell (Blaustein & Lederer 1999;Hryshko, 2002;Bers et al 2003). Because both sarcolemmal Ca 2+ channels and the Na + -Ca 2+ exchanger are voltage dependent, changes in either resting membrane potential J Physiol 556.3 or action potential waveform are expected to significantly alter Ca 2+ fluxes via these pathways.…”