During rodent ventricular cell development, the sarcoplasmic reticulum (SR) is scarce and poorly organized. A Ca2+ transient in embryonic ventricular cells depends mostly on Ca2+ influx through L-type Ca2+ channels. In rat ventricular cells, transverse tubules (t-tubules) begin to form postnatally. As such, Ca2+-induced Ca2+ release (CICR), in which ryanodine receptor channels on the SR are activated via Ca2+ influx through L-type Ca2+ channels on the t-tubules, is not established in embryonic ventricular cells. Here, we modeled developmental changes in Guinea pig ventricular cells and identified the factors that enhance contraction of the cells with an increase in CICR.