Objective:To study the effect of salvianolic acid A(SAA) on L-type calcium current(l-CaL) in isolated ventricular myocytes of Sprague-Dawley rats.Methods:SAA powder was dissolved in normal Tyrode’s solution to reach the concentrations of 1,10,100,and 1000μmol/L.The traditional whole-cell patch-clamp recording technique was employed to evaluate the effects of SAA on 1-CaL in single ventricular myocytes which were prepared by Langendorff perfusion apparatus from Sprague-Dawley rats.Results:SAA(1,10,100, and 1000μmol/L) inhibited l-CaL peak value by 16.23%±1.3%(n=6,P<0.05),22.9%±3.6%(n=6,P<0.05), 53.4%±3.0%(n=8,P<0.01),and 62.26%±2.9%(n=6,P<0.01),respectively.SAA reversibly inhibited l-CaL in a dose-dependent manner and with a half-blocking concentration(IC_(50)) of 38.3μmol/L.SAA at 100μmol/L elevated theⅠ-Ⅴcurve obviously,and shifted the half-active voltage(V_(0.5)) from(-15.78±0.86) mV to(-11.24±0.77) mV(n=6,P<0.05) and the slope(K) from 5.33±0.74 to 4.35±0.74(n=6,P>0.05).However,it did not alter the shapes ofⅠ-Ⅴcurve,steady-state inactivation curve,or recovery from inactivation curve.Conclusions: SAA inhibited l-CaL in a dose-dependent manner.It shifted the steady-state activation curve to a more positive voltage,which indicated that the drug affected the activated state of calcium channels,and suggested that the Ca~(2+) antagonistic effect of SAA be beneficial in the treatment of myocardial ischemia reperfusion injury. Objective: To study the effect of salvianolic acid A (SAA) on L-type calcium current (l-CaL) in isolated ventricular myocytes of Sprague-Dawley rats. Methods: SAA powder was dissolved in normal Tyrode’s solution to reach the concentrations of 1 , 10,100, and 1000 μmol / L. The traditional whole-cell patch-clamp recording technique was employed to evaluate the effects of SAA on 1-CaL in single ventricular myocytes which were prepared by Langendorff perfusion apparatus from Sprague-Dawley rats. Results: SAA (1, 10, 100, and 1000μmol / L) inhibited l-CaL peak value by 16.23% ± 1.3% (n = 6, P <0.05), 22.9% ± 3.6% 3.0% (n = 8, P <0.01), and 62.26% ± 2.9% (n = 6, P <0.01), respectively.SAA reversibly inhibited 1-CaL in a dose-dependent manner and with a half-blocking concentration IC 50 of 38.3 μmol / L SAAA at 100 μmol / L elevated the I-Vcurve obviously, and shifted the half-active voltage V_ (0.5)) from -15.78 ± 0.86 mV to (-11.24 ± 0.77) mV (n = 6, P <0.05) and the slope (K) from 5.33 ± 0.74 to 4.35 ± 0.74 (n = 6, P> Steady-state inactivation curve, or recovery from inactivation curve. Conclusions: SAA inhibited l-CaL in a dose-dependent manner. It shifted the steady-state activation curve to a more positive voltage, which indicates that the drug affected the activated state of calcium channels, and suggested that the Ca 2+ antagonistic effect of SAA be beneficial in the treatment of myocardial ischemia reperfusion injury.