Developmental differences in myocardial transmembrane Na+ transport:

Resting intracellular Na+ concentration ([Na+]i), measured in freshly isolated rat ventricular myocytes with CoroNa green, was not significantly different in neonates (3–5 days old) and adults, but electrical stimulation caused marked [Na+]i rise only in neonates. Inhibition of L-type Ca2+ current by CdCl2 abolished not only systolic Ca2+ transients, but also activity-dependent intracellular Na+ accumulation in immature cells.

This indicates that the main Na+ influx pathway during activity is the Na+/Ca2+ exchanger, rather than voltage-dependent Na+ current (INa), which was not affected by CdCl2. In immature myocytes, INa density was two-fold greater, inactivation was faster, and the current peak occurred at less negative transmembrane potential (Em) than in adults. Na+ channel steady-state activation and inactivation curves in neonates showed a rightward shift, which should increase channel availability at diastolic Em, but also require greater depolarization for excitation, which was observed experimentally and reproduced in computer simulations.