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.