Cardiac function is critically dependent on the movement of ions across membranes. Contraction of the heart begins when an action potential depolarizes the plasma membrane of the myocyte, the sarcolemma. Depolarization is caused by sequential inward currents of sodium ions and calcium ions. The slow inward calcium current enters through voltagegated channels in the sarcolemma and serves several purposes. First, this current supplies a small amount of the activator calcium for binding to troponin C. Second, the sarcoplasmic reticulum (SR) takes up a considerable portion of this calcium, where it forms part of the internal store for release in subsequent contractions. Finally, this calcium triggers the release of a large amount of calcium from the SR. The released SR calcium initiates contraction by binding to troponin C, resulting in formation of cross-bridges between the myosin head and actin. Relaxation begins with the removal of calcium from the myofilaments, which is mediated primarily by the SR calcium pump but also by the Na+-Ca2+ exchanger. Removal of calcium from the myofilaments results in the breaking of actin-myosin cross-bridges and return to the resting state.

Important changes in the structure and function of cardiac membranes occur during maturation of the mammalian heart (and probably in all vertebrate hearts). These changes result in significant age-related differences in myocardial function. This chapter discusses recent work that has increased our understanding of developmental changes in cardiac membranes and of the impact of these changes on myocardial performance.