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Combination of quantitative changes in ionic components to enhance the contractile force during T-tubule development

During rodent ventricular cell development, the sarcoplasmic reticulum (SR) is scarce and poorly organized. A Ca<sup>2+</sup> transient in embryonic ventricular cells depends mostly on Ca<sup>2+</sup> influx through L-type Ca<sup>2+</sup> channels. In rat ventricular cells, transverse tubules (t-tubules) begin to form postnatally. As such, Ca<sup>2+</sup>-induced Ca<sup>2+</sup> release (CICR), in which ryanodine receptor channels on the SR are activated via Ca<sup>2+</sup> influx through L-type Ca<sup>2+</sup> 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.