In human endothelial cells, physiological concentrations of estrogen stimulated a rapid release of nitric oxide and increased intracellular calcium concentration through the activation of a cell surface receptor (Stefano et al. 2000). Estrogen–induced intracellular translocation of eNOS was preceded by a transient increase in intracellular calcium in endothelial cells (Goetz et al. 1999). In addition, conjugated estrogen induced a rapid and sustained increase in intracellular calcium concentrations in human spermatozoa and this was dependent on extracellular calcium (Luconi et al. 1999). Moreover, the conjugated estrogen–increased intracellular calcium concentration was correlated with prolactin release in rat prolactinoma cells, which highly expressed membrane ER. Estrogen has been reported to mediate Ca2+ flux in astrocytes through a membrane–associated ER that activated phospholipase C pathway (Chaban et al. 2004). The conjugated estrogen inhibited intracellular calcium release in dorsal root ganglia neurons. This attenuation of intracellular Ca2+ transient was mediated by estrogen action through voltage gated Ca2+ channels (VGCC) (Chaban et al. 2003).