a tight coupling between cell structure, ionic fluxes and intracellular ca2+ transients underlies the regulation of cardiac cell function. to investigate how a distribution of ca2+ handling proteins may affect these coupled processes we developed a 3-d model of ca2+-signaling, buffering and diffusion in rat ventricular myocytes. the model geometry was derived from the experiment. a diffusion modeling software using finite element tool kit (fetk) libraries was implemented to solve the 4 coupled pde systems. we concluded that the cardiac cell function is tightly regulated by the localization of ca2+-handling proteins and strongly relays on the presence of mobile and stationary ca2+ buffers and cell geometry.