Influence of cyclovirobuxine D on intracellular [Ca(2+)] regulation and the expression of the calcium cycling proteins in rat myocytes.

Our previous studies have shown that cyclovirobuxine D (CVB-D) ameliorated the cardiac function in heart failure rats. Considering the relationship between cardiac function and [Ca(2+)]i, and the role of calcium cycling on regulating [Ca(2+)]i, the present study was designed to evaluate the influence of CVB-D on the calcium transient of myocytes from neonatal rats and adult heart failure (HF) rats. The expression of calcium cycling proteins, including L-type calcium channel (LTCC), ryanodine receptor 2 (RYR2), sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) and sodium-calcium exchanger (NCX), were investigated to explore the underlying mechanism. CVB-D increased the intensity of calcium transient, accelerated the process of calcium transient and attenuation in the neonatal and adult myocytes. Furthermore, CVB-D shortened T(peak) and T(attenuation) in the adult myocytes and slowed down the heart rate of neonatal myocytes. Besides, CVB-D increased the expression of RYR2 and SERCA2a, decreased the expression of NCX, but showed no significant effect on LTCC. Thus, it was concluded that CVB-D increased the release and uptake of Ca(2+) in systolic and diastolic period, respectively. CVB-D might not only facilitate the utilization of intracellular Ca(2+), but also prevent the loss of Ca(2+).