Ca2+ regulates the kinetics of tension development in intact cardiac muscle.

The goal of this study was to determine whether Ca2+ plays a role in regulating tension development kinetics in intact cardiac muscle. In cardiac muscle, this fundamental issue of Ca2+ regulation has been controversial. The approach was to induce steady-state tetanic contractions of intact right ventricular trabeculae from rat hearts at varying external Ca2+concentrations ([Ca2+]) at 22°C. During tetani, cross bridges were mechanically disrupted and the kinetics of tension redevelopment were assessed from the rate constant of exponential tension redevelopment ( k tr). There was a relationship between k tr and external [Ca2+] that was similar in form to the relationship between tension and [Ca2+]. Thus a close relationship also existed between k tr and tension ( r = 0.88; P < 0.001); whereas at maximal tetanic tension (saturating cytosolic [Ca2+]), k tr was 16.4 ± 2.2 s-1 (mean ± SE, n = 7), at zero tension (low cytosolic [Ca2+]), k tr extrapolated to 20% of maximum (3.3 ± 0.7 s-1). Qualitatively similar results were obtained using different mechanical protocols to disrupt cross bridges. These data demonstrate that tension redevelopment kinetics in intact cardiac muscle are influenced by the level of Ca2+ activation. These findings contrast with the findings of one previous study of intact cardiac muscle. Activation dependence of tension development kinetics may play an important role in determining the rate and extent of myocardial tension rise during the cardiac cycle in vivo.