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Journal of Korean Neurosurgical Society 1997;26(12): 1644-1652. |
| The Effect Erythrocyte lysate on Intracellular Calcium Concentration and the Potassium Channel in Cerebral Vasular Smooth Muscle Cells. |
| Chul Jin Kim |
| Department of Neurosurgery, Chonbuk National University School of Medicine, Chonju, Korea. |
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| ABSTRACT |
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Erythrocyte lysate increases intracellular Ca2+[Ca2+]i, causes contraction in cerebral arteries, and is thought to be the causative agent in cerebral vasospasm ; the mechanism of erythrocyte lysate-induced [Ca2+]i mobilization is not, however, clear. This study was undertaken to investigate the action of erythrocyte lysate on [Ca2+]i mobilization by monitoring [Ca2+]i and the Ca2+-dependent K+ channels(Kca) in freshly isolated rat basilar artery smooth muscle cells. In a [Ca2+]i imaging study, erythrocyte lysate produced a biphasic response, a transient peak and prolonged plateau [Ca2+]i elevation ; in the absence of external Ca2+, it induced only a transient peak [Ca2+]i response without a marked plateau phase, indicating that peak [Ca2+]i was due to Ca2+ released from internal stores. The erythrocyte lysate-induced plateau [Ca2+]i response was resistant to nicardipine, a voltage-dependent Ca2+ channel blocker, but was abolished by EGTA. The elevation [Ca2+]i induced by erythrocyte lysate caused contraction in smooth muscle cells. During the electrophysiological study, elevation of [Ca2+]i by erythrocyte lysate increased Kca currents in whole-cell patch-clamp configuration ; this effect was blocked by heparin, an antagonist of IP3 receptors. We conclude that erythrocyte lysate releases Ca2+ from IP3-sensitive intracellular stores and induces Ca2+ entry from voltage-independent Ca2+ pathways. |
| Key Words:
Erythrocyte lysate; K+ channels; IP3; [Ca2+]i; Vasospasm; Cerebral smooth muscle cells |
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