Hancock W O, Martyn D A, Huntsman L L
Center for Bioengineering, University of Washington, Seattle 98195.
Circ Res. 1993 Oct;73(4):603-11. doi: 10.1161/01.res.73.4.603.
The influence of Ca2+ and sarcomere length on myocardial crossbridge kinetics was studied in ferret papillary muscle by measuring the rate of force redevelopment following a rapid length step that dropped the force to zero. Tetanic stimulation with 5 mumol/L ryanodine was used to obtain a steady-state contraction, and segment length was measured and controlled using a sense-coil technique that measures changes in the cross-sectional area of the central region of the muscle. The rate constant for the recovery of force (ktr) following a rapid length release was obtained by fitting the data with a single exponential function. Contrary to results from skinned skeletal fibers in which ktr increases almost 10-fold from low to maximal activation levels, ktr was found not to increase at higher activation levels in this study. Similarly, although force increased with segment length under all conditions, ktr never increased with length. Data presented here are consistent with a model of myocardial Ca2+ activation in which Ca2+ modulates the number of crossbridges interacting with the thin filament and are inconsistent with a model in which Ca2+ modulates the kinetics of transitions to force producing states within the actomyosin cycle. Differences in the activation dependence of the force redevelopment rate between cardiac and skeletal muscle suggest that there are fundamental differences in the mechanism of Ca2+ activation between these two muscle types.
通过测量快速长度阶跃(使力降至零)后力重新恢复的速率,研究了钙离子(Ca2+)和肌节长度对雪貂乳头肌心肌横桥动力学的影响。使用5微摩尔/升的雷诺丁进行强直刺激以获得稳态收缩,并使用测量肌肉中心区域横截面积变化的感应线圈技术来测量和控制节段长度。通过用单指数函数拟合数据,获得快速长度释放后力恢复的速率常数(ktr)。与去皮肤骨骼肌纤维的结果相反,在去皮肤骨骼肌纤维中ktr从低激活水平到最大激活水平增加近10倍,而在本研究中发现ktr在较高激活水平下并未增加。同样,尽管在所有条件下力都随节段长度增加,但ktr从未随长度增加。此处给出的数据与心肌Ca2+激活模型一致,在该模型中Ca2+调节与细肌丝相互作用的横桥数量,并且与Ca2+调节肌动球蛋白循环中向产生力状态转变动力学的模型不一致。心肌和骨骼肌之间力重新恢复速率的激活依赖性差异表明,这两种肌肉类型在Ca2+激活机制上存在根本差异。