Reversal of caldesmon function by anti-caldesmon antibodies confirms its role in the calcium regulation of vascular smooth muscle thin filaments.

Direct evidence that caldesmon is the Ca2+-regulated inhibitory component of native smooth muscle thin filaments is provided by studies using caldesmon-specific antibodies as antagonists. The antibodies reverse caldesmon inhibition of actomyosin ATPase and abolish Ca2+-regulation of native aorta thin filament activation of myosin ATPase. This effect is a result of antibody binding to the caldesmon on the filament thereby inactivating it and not due to antibody-induced caldesmon dissociation from the filament. The antibodies, however, neutralise caldesmon only in systems using skeletal muscle myosin and not in those using smooth muscle myosin; this implies that smooth muscle myosin prevents appropriate antibody binding to caldesmon perhaps because smooth muscle myosin binds to caldesmon thus preventing access of antibody to antigenic sites.