We aim at clarifying the role of individual ion channels in the cardiac cell function by constructing a comprehensive cell model (Kyoto Model) based on the cardiac cell model developed by DiFrancesco and Noble (1985), the sarcomere contraction model by Negroni and Lascano (1996) and the mitochondria oxidative phosphorylation model by Korzeniewski and Zoladz (2001). To access the central role of L-type Ca²⁺ channel (I_CaL), the model of Ca²⁺-dependent inactivation developed by Shirokov et al (1993) was used. The amplitude factor of I_CaL was adjusted to simulate the I_CaL recorded by the action potential clamp experiment by Linz and Meyer (1998). The gating kinetics of the Ca²⁺-releasing (RyR) channel of the sarcoplasmic reticulum (SR) (Hilgemann & Noble, 1987) was adjusted to give the staircase phenomena of single cell contraction, and the time course of Ca²⁺ transient was adjusted based on the experimental measurements of SR Ca²⁺ release, Ca²⁺ leak and Ca²⁺ pump uptake (Wier et al., 1994). The Ca²⁺-gain, which is given as the ratio of peak Ca²⁺ fluxes via IRyR to that of I_CaL is in the range of experimental measurements reported by Wier et al (1994). The Kyoto model well reconstructed the positive inotropy as well as the shortening of the action potential at higher [Ca²⁺]o, and revealed the time-dependent changes in the open probability of Ca²⁺ gate of I_CaL in the ventricular cell model. The same Ca²⁺-dependent gate of I_CaL also took the pivotal role in the sinoatrial node cell model when reconstructing the increase of the pacemaker rhythm accompanied with the action potential shortening with increasing [Ca²⁺]o. The role of Cl^– channels was assessed by including a hypothetical and background Cl^– channel in the Kyoto model. The intracellular [Cl^–]i homeostasis was established by implementing the Na⁺,K⁺,2Cl^– cotransporter model developed by Benjamin & Johnson (1997). Increasing the membrane Cl^– conductance, simulating the activation of the cAMP-dependent Cl^– channel, the cell volume was decreased with a membrane depolarization of a few mV as observed in the experiment (Wang et al., 1997, Sasaki et al. 1999). If the Na⁺/K⁺ pump was blocked, the cell volume gradually increased. The model revealed that this volume increase was in parallel to the net Cl^– influx caused by membrane depolarization via redistribution of K⁺ across the cell membrane. The model indicated that the Cl^– flux takes the central role in the acute phase of cell volume regulation.