Erythrocyte lysate releases Ca2+ from IP3-sensitive stores and activates Ca2+ -dependent K+ channels in rat basilar smooth muscle cells

Abstract

Erythrocyte lysate increases intracellular Ca2+ ([Ca2+ Ji), contracts cerebral arteries and has been suggested to be the causative agent for cerebral vasospasm. However, the mechanism of erythrocyte lysate-induced [Ca2+ Ji mobilization is not clear. This study was undertaken to investigate the action of erythrocyte lysate on [Ca2+ Ji mobilization by monitoring [Ca2+ Ji and the Ca2+ -dependent K+ channels (Kca) in freshly isolated rat basilar artery smooth muscle cells. In a [Ca2+ Ji ima3ing study, erythrocyte lysate produced a biphasic response, a transient peak and a prolonged plateau rCa + Ji elevation. In the absence of external Ca2+ erythrocyte lysate induced only a transient peak [Ca2+ Ji response without a marked plateau phase, indicating the [Ca2+ Ji was Ca2+ released from internal stores. Erythrocyte lysate-induced plateau [Ca2+Ji response was resistant to nicardipine, a voltage-dependent Ca2+ channel blocker, but was abolished by ECTA. Elevation of [Ca2+ Ji induced by erythrocyte lysate contracted smooth muscle cells. In the electrophysiological study, elevation of [Ca2+ Ji by erythrocyte lysate increased KCa currents in whole-cell patch-clamp configuration. This effect of erythrocyte lysate on Kca was blocked by heparin, an antagonist of IPj receptors. We conclude that erythrocyte lysate releases Ca2+ from IPj-sensitive intracellular stores and produces Ca2+ entry from voltage-independent Ca2+ pathways. [Neural Res 1998; 20: 23–30]