ERYTHROCYTE LYSATE RELEASES CA2-SENSITIVE STORES AND ACTIVATES CA2+-DEPENDENT K+ CHANNELS IN RAT BASILAR SMOOTH-MUSCLE CELLS( FROM IP3)

Erythrocyte lysate increases intracellular Ca2+ ([Ca2+](i)), contracts cerebral arteries and has been suggested to be the causative agent fo r cerebral vasospasm. However, the mechanism of erythrocyte lysate-ind uced [Ca2+](i) mobilization is not clear. This study was undertaken to investigate the action of erythrocyte lysate [Ca2+](i) mobilization b y monitoring [Ca2+](i) and the Ca2+-dependent K+ channels (K-Ca) in fr eshly isolated rat basilar artery smooth muscle cells. In a [Ca2+](i) imaging study, erythrocyte lysate produced a biphasic response, a tran sient peak and a prolonged plateau [Ca2+](i) elevation. In the absence of external Ca2+, erythrocyte lysate induced only a transient peak [C a2+](i) response without a marked plateau phase, indicating the [Ca2+] (i) was Ca2+ released from internal stores. Erythrocyte lysate-induced plateau [Ca2+](i) response was resistant to nicardipine, a voltage-de pendent Ca2+ channel blocker, but was abolished by EGTA. Elevation of [Ca2+](i) induced by erythrocyte lysate contracted smooth muscle cells . In the electrophysiological study, elevation of [Ca2+](i) by erythro cyte lysate increased K-Ca currents in whole-cell patch-clamp configur ation. This effect of erythrocyte lysate on K-Ca was blocked by hepari n, an antagonist of IP3 receptors. We conclude that erythrocyte lysate releases Ca2+ from IP3-sensitive intracellular stores and produces Ca 2+ entry from voltage-independent Ca2+ pathways.