17 beta-estradiol induces L-type Ca2+ channel activation and regulates redox function in macrophages

17 beta-estradiol induces rapid effects on cells of the immune system via plasma membrane surface receptor but the ways in which delayed signals involving intracellular receptors affect the same functions are not well understood. To study the delayed but sustained events in estradiol signaling, we have investigated macrophage Ca(2+) signaling, detected specific Ca(2+) ion channel activated and found a relationship between intracellular calcium [Ca(2+)](i) and macrophage release of reactive oxygen species (ROS) and nitric oxide (NO) during delayed 17 beta-estradiol activity. We found evidence of additional effect of estradiol on capacitative entry of Ca(2+), Ca(2+) entry through L-type channel and a direct relationship between [Ca(2+)](i) and generation of ROS and NO. This study demonstrates that 17 beta-estradiol exhibits a delayed phase of Ca(2+) influx involving L-type channel and regulates macrophage immune redox function.