Many studies describe the stimulating eff ect ofquercetin on Ca 2+ channels and the treatment of cardiovasculardiseases such as myocardial ischemia and hypertension. However, these studies are scattered and contradictory. The aim of this study is to elucidate the protective eff ects ofquercetin against isoproterenol (ISO)-induced myocardialischemia and verify the cellular mechanisms based on theL-type Ca 2+ channel (LTCC), Ca 2+ transients, and myocardialcontractility. An animal model of myocardial ischemiawas established by subcutaneous injection of ISO for 2 days. Quercetin significantly reduced J-point elevation, heartrate, reactive oxygen species, serum levels of myocardialenzymes, superoxide dismutase, catalase, glutathione, glutathioneperoxidase, glutathione S-transferase and improvedheart pathologic morphology. L-type Ca 2+ current (I Ca-L )was tested in an experiment with isolated rat myocardialcells by using the whole-cell patch-clamp recording techniqueand IonOptix Myocam detection system. Quercetin reduced I Ca-L in a concentration-dependent fashion with ahalf-maximal inhibitory concentration of 4.67 × 10 –4 M. Quercetin also shifted the current–voltage curve upwards,moved the activation and inactivation curves to the left andinhibited the amplitude of the cell shortening and Ca 2+ transients. The results showed that quercetin acts as a LTCCinhibitor and exerts a cardioprotective eff ect by inhibitingCa 2+ infl ux and contractility in rats.