[ $(1R,9S)-{eta} ]-Hydrastine$ (BHS), at $100{mu}M$, has been shown to mainly reduce the $K^+-induced$ dopamine release and $Ca^{2+}$ influx by blocking the L-type $Ca^{2+}$ channel and inhibit the caffeine activated store-operated $Ca^{2+}$ channels, but not those activated by thapsigargin, in PC12 cells. In this study, the effects of BHS on $Ca^{2+}$ transport from $Ca^{2+}$ stores in the absence of external $Ca^{2+}$ were investigated in PC12 cells. BHS decreased the basal intracellular $Ca^{2+}$ concentration $([Ca^{2+}]_i)$ in the absence of external $Ca^{2+}$ in PC12 cells. In the absence of external $Ca^{2+}$, pre-treating PC12 cells with $100{mu}M$ BHS reduced the rapid increase in the $[Ca^{2+}]_i$ elicited by 20mM caffeine, but not that by $1{mu}M$ thapsigargin. In addition, BHS inhibited the increase in the $[Ca^{2+}]_i$ elicited by restoration of 2mM $CaCl_2$ after the $Ca^{2+}$ stores had been depleted by 20mM caffeine, but not those depleted by $1{mu}M$ thapsigargin, in the absence of external $Ca^{2+}$. These results suggested that BHS mainly inhibited $Ca^{2+}$ leakage from the $Ca^{2+}$ stores and the caffeine-stimulated release of $Ca^{2+}$ from the caffeine-sensitive $Ca^{2+}$ stores in PC12 cells.