THE TIME-COURSE OF MYOSIN LIGHT-CHAIN PHOSPHORYLATION IN BLOOD-INDUCED VASOSPASM

被引:31
作者
HARADA, T
SETO, M
SASAKI, Y
LONDON, S
LUO, ZY
MAYBERG, M
机构
[1] UNIV WASHINGTON,DEPT NEUROL SURG,SEATTLE,WA 98195
[2] ASAHI CHEM IND CO LTD,BIOCHEM RES LAB,MIYAZAKI,JAPAN
关键词
CALCIUM; CEREBRAL ARTERY; MYOSIN LIGHT CHAIN; SUBARACHNOID HEMORRHAGE; VASOSPASM;
D O I
10.1227/00006123-199506000-00018
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
THE PHOSPHORYLATION OF an M(r) 20,000 myosin light chain (MLC(20)) promotes the generation of contractile force through actin-myosin adenosine triphosphatase in most agonist-mediated vascular smooth muscle cell contraction. However, the role of calcium-mediated contractile processes in sustained arterial narrowing after subarachnoid hemorrhage remains unknown. In a femoral artery model of vasospasm, whole blood was applied to arteries in 54 rats for periods of 2 to 10 days; the contralateral artery treated with platelet-rich plasma served as matched control. During the early stage of vasospasm (Days 2-5), in the media of arteries exposed to blood, MLC(20) phosphorylation (including diphosphorylated forms) increased significantly (30-38%; P < 0.05); total medial MLC(20) during this interval was comparable to that in controls. After 5 days, however, total MLC(20) decreased markedly (>90%; P < 0.01) compared with controls; phosphorylated MLC(20) was undetectable during this interval. MLC(20)-mediated contractile processes may be prominent in the early stages of arterial narrowing after subarachnoid hemorrhage; later stages are associated with the loss of MLC(20) and the possible persistence of arterial narrowing by other mechanisms.
引用
收藏
页码:1178 / 1182
页数:5
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