Ca2+ modulates both the number and the kinetics of force-generating crossbridges in cardiac muscle, similar to skeletal muscle.
OBJECTIVES: The effects of Ca2+ on the rate of tension redevelopment following a brief release/restretch were investigated in single chemically-skinned ventricular myocytes from the rat. METHODS: The myocytes were enzymatically isolated and skinned using Triton-X100. They were then attached with an optical adhesive glue to glass micropipettes fixed to a piezoelectric translator and a force transducer. Tension redevelopment was measured at various levels of Ca activation after disrupting force-generating crossbridges by a brief (20 ms) step release/restretch equivalent to 20% of the original 2.1 microns sarcomere length. Most of tension redevelopment was well fitted by a monoexponential function. RESULTS: At maximal Ca concentrations, pCa 4.5 maximal force was obtained at 2.1 microns sarcomere length and averaged 11.8 +/- 0.7 microN. The rate of tension redevelopment (ktr) increased with increasing Ca concentrations up to 5.19 +/- 0.37.s-1 at maximal Ca activation. The relation between the rate of tension redevelopment and Ca concentration was sigmoidal and could be fitted by the Hill equation with coefficients similar to those describing the tension-pCa relation. The relation between relative rate of tension redevelopment and relative steady activated tension was curvilinear increasing with increasing Ca concentration. CONCLUSIONS: In cardiac muscle, Ca2+ modulates both the number and the kinetics of force-generating crossbridges in a manner similar to that previously reported in skeletal muscle.
Vannier et al. (Sun,) studied this question.