Before revision:  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. This work, together with the recent study by Hannanta-anan and Chow, suggests a ]  plausible mechanism for IP3-dependent hypertrophic signalling in cardiomyocytes.
After revision:  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. Furthermore we demonstrate that IP3-mediated Ca2+ release in the cytosol increases the duty cycle of the Ca2+ transient, the fraction of the cycle for which ] plausible mechanism for IP3-dependent hypertrophic signalling in cardiomyocytes.