The results obtained in the present study indicate that pharmacological modulation of Ca2+/cAMP/ADO signaling in cardiac cells by means of the attenuation of Ca2+ influx via LTCC and the activation of A1R by endogenous ADO could be a promising therapeutic strategy to reduce the incidence of severe and fatal arrhythmias caused by AMI in humans. Here, ADO is linked to cardiac arrhythmia.