CALMIDAZOLIUM ALTERS CA2-MUSCLE( REGULATION OF TENSION REDEVELOPMENT RATE IN SKINNED SKELETAL)

To examine if the Ca2+-binding kinetics of troponin C (TnC) can influe nce the rate of cross-bridge force production, we studied the effects of calmidazolium (CDZ) on steady-state force and the rate of force red evelopment (k(tr)) in skinned rabbit psoas muscle fibers. CDZ increase d the Ca2+-sensitivity of steady-state force and k(tr) at submaximal l evels of activation, but increased k(tr) to a greater extent than can be explained by Increased force alone, This occurred in the absence of any significant effects of CDZ on solution ATPase or in vitro motilit y of fluorescently labeled F-actin, suggesting that CDZ did not direct ly influence cross-bridge cycling CDZ was strongly bound to TnC in aqu eous solutions, and its effects on force production could be reversed by extraction of CDZ-exposed native TnC and replacement with purified (unexposed) rabbit skeletal TnC. These experiments suggest that the me thod of CDZ action in fibers is to bind lo TnC and increase its Ca2+-b inding affinity, which results in an increased rate of force productio n at submaximal [Ca2+]. The results also demonstrate that the Ca2+-bin ding kinetics of TnC influence the kinetics of k(tr).