The ryanodine receptor type 2 (RyR‐2) functions as a Ca 2+‐induced Ca 2+ release (CICR) channel on intracellular Ca 2+ stores and is distributed in most excitable cells with the exception of skeletal muscle cells. RyR‐2 is abundantly expressed in cardiac muscle cells and is thought to mediate Ca 2+ release triggered by Ca 2+ influx through the voltage‐gated Ca 2+ channel to constitute the cardiac type of excitation–contraction (E–C) coupling. Here we report on mutant mice lacking RyR‐2. The mutant mice died at approximately embryonic day (E) 10 with morphological abnormalities in the heart tube. Prior to embryonic death, large vacuolate sarcoplasmic reticulum (SR) and structurally abnormal mitochondria began to develop in the mutant cardiac myocytes, and the vacuolate SR appeared to contain high concentrations of Ca 2+. Fluorometric Ca 2+ measurements showed that a Ca 2+ transient evoked by caffeine, an activator of RyRs, was abolished in the mutant cardiac myocytes. However, both mutant and control hearts showed spontaneous rhythmic contractions at E9. 5. Moreover, treatment with ryanodine, which locks RyR channels in their open state, did not exert a major effect on spontaneous Ca 2+ transients in control cardiac myocytes at E9. 5–11.5. These results suggest no essential contribution of the RyR‐2 to E–C coupling in cardiac myocytes during early embryonic stages. Our results from the mutant mice indicate that the major role of RyR‐2 is not in E–C coupling as the CICR channel in embryonic cardiac myocytes but it is absolutely required for cellular Ca 2+ homeostasis most probably as a major Ca 2+ leak channel to maintain the developing SR.