IMMUNOBLOTTING OF CONTRACTILE AND CYTOSKELETAL PROTEINS OF CANINE BASILAR ARTERY IN VASOSPASM

VASOSPASM WAS PRODUCED in the canine basilar arteries by a two-hemorrh age method, and voltage- and receptor-dependent contractions of the no rmal canine basilar arteries were induced by local applications of pot assium chloride (KCl) and serotonin, respectively, after transclival e xposure. Actin, myosin, desmin, filamin, talin, vinculin, and alpha-ac tinin in the basilar artery were studied by immunoblotting. The immuno blots showed a decrease or loss in immunoreactivity of some native pro teins and generation of protein fragments, smaller in size than native proteins, in spastic, KCl, and serotonin groups, indicating a proteol ytic degradation. In the spastic group on Day 2, actin, desmin, and fi lamin were usually degraded slightly; myosin moderately; and talin and alpha-actinin substantially. Vinculin and metavinculin remained intac t. In the spastic group on Day 7, actin and desmin were usually decomp osed slightly; myosin, filamin, and vinculin substantially; and talin, metavinculin, and alpha-actinin markedly. In the KCl and serotonin gr oups, slight degradation was usually observed in filamin, often in alp ha-actinin, and occasionally in actin, whereas desmin, vinculin, and m etavinculin were not degraded. In addition, myosin was usually degrade d moderately in the KCl group and slightly in the serotonin group, and talin was generally decomposed slightly in the KCl group and moderate ly in the serotonin group. The degraded fragments, although variable i n number and immunoreactivity, were similar in size in the three group s. We suggest that the intracellular devices responsible for contracti on of the basilar arteries are degraded more severely in the spastic g roup than in the KCl or serotonin group, probably by similar proteolyt ic mechanism and progressively with the passage of time after subarach noid hemorrhage in vasospasm.