Before revision:  Here we present a mathematical model of functional interactions between RyR and IP3R channels which demonstrates that IP3-mediated Ca2+ release in the cytosol is indeed capable of increasing the duty cycle of the calcium signal in the cardiomyocyte. Through comparison with published experimental results we demonstrate the importance of appropriately representing IP3R gating, verify that our model is capable of reproducing known disease phenotypes in the calcium transientthrough alteration of channel properties , and examine how sensitive the cardiac cell is to IP3 . A key result of our study is that increasing IP3 concentration increases calcium transient duration but may not always lead to positive inotropy.
After revision:  Here we present a mathematical model of functional interactions between RyR and IP3R channels which demonstrates that IP3-mediated Ca2+ transient , and examine how sensitive the cardiac cell is to IP3 . A key result of our study is that increasing IP3 concentration increases calcium transient duration but may not always lead to positive inotropy.