We have studied the post-natal maturation of excitation-contraction coupling in rat ventricle by means of pharmacological agents that selectively modulate either Ca entry via voltage-dependent sarcolemmal channels (dihydropyridines) or Ca release from sarcoplasmic reticulum (ryanodine). We have investigated the effects of those agents on cardiac contractility, and we have used them as radioligands to examine the properties of their receptors. Our results show that, after birth, dihydropyridine receptors (i.e. voltage-dependent Ca channels) redistribute to transverse tubules, in close proximity of terminal cisternae of sarcoplasmic reticulum. This redistribution favors the mechanism whereby, in adult ventricle, extracellular Ca entry triggers Ca release from sarcoplasmic reticulum.