Protective effect of quercetin against myocardial ischemia as a Ca2+ channel inhibitor: involvement of inhibiting contractility and Ca2+ influx via L-type Ca2+ channels.

Many studies describe the stimulating effect of quercetin on Ca2+ channels and the treatment of cardiovascular diseases such as myocardial ischemia and hypertension. However, these studies are scattered and contradictory. The aim of this study is to elucidate the protective effects of quercetin against isoproterenol (ISO)-induced myocardial ischemia and verify the cellular mechanisms based on the L-type Ca2+ channel (LTCC), Ca2+ transients, and myocardial contractility. An animal model of myocardial ischemia was established by subcutaneous injection of ISO for 2 days. Quercetin significantly reduced J-point elevation, heart rate, reactive oxygen species, serum levels of myocardial enzymes, superoxide dismutase, catalase, glutathione, glutathione peroxidase, glutathione S-transferase and improved heart pathologic morphology. L-type Ca2+ current (ICa-L) was tested in an experiment with isolated rat myocardial cells by using the whole-cell patch-clamp recording technique and IonOptix Myocam detection system. Quercetin reduced ICa-L in a concentration-dependent fashion with a half-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 and inhibited the amplitude of the cell shortening and Ca2+ transients. The results showed that quercetin acts as a LTCC inhibitor and exerts a cardioprotective effect by inhibiting Ca2+ influx and contractility in rats.