Changes in force and cytosolic Ca2+ concentration after length changes in isolated rat ventricular trabeculae
Changes in force and cytosolic Ca2+ concentration after length changes in isolated rat ventricular trabeculae
复制标题
DOI：
10.1111/j.1469-7793.1998.431bw.x
复制
发表时间：
1998-01-15
影响因子：
5.5
通讯作者：
Wrzosek, A
中科院分区：
文献类型：
--
作者：
Kentish, JC;Wrzosek, A
1. 在微注射fura-2盐的离体大鼠小梁中测量胞浆[Ca2+]（[Ca2+](i)）的变化，以研究肌肉长度改变后抽搐力变化的机制。肌肉长度的一步增加会产生快速的抽搐力增强，但不会产生Ca2+瞬态。2 . ryanodine和cyclopiazonic acid对肌浆网（SR）的抑制不影响力的快速上升。从sr抑制肌肉的抽搐和强直性收缩中确定的肌原纤维原位的力-[Ca2+](i)关系表明，力的快速上升主要是由于肌原纤维Ca2+敏感性的增加，以及肌原纤维最大力生产的增加。拉伸肌肉后，抽搐力进一步缓慢增加，这完全是由于Ca2+瞬态的缓慢增加，因为肌纤维力-[Ca2+](i)关系没有变化。SR抑制减缓了慢力反应，但没有改变慢力反应的大小。在缓慢上升的力，没有缓慢增加舒张[Ca2+](i)，无论是否抑制SR。在未受刺激的肌肉中也是如此。我们得出结论，肌肉拉伸后抽搐力的快速增加是由于肌原纤维的长度依赖特性。缓慢的力增加不能用肌原纤维或SR的长度依赖性来解释，也不能用舒张[Ca2+]的升高来解释(i)。来自破伤风的证据表明，缓慢的力反应是由于在动作电位期间细胞Ca2+负荷增加所致。
1. Changes in cytosolic [Ca2+] ([Ca2+](i)) were measured in isolated rat trabeculae that had been micro-injected with fura-2 salt, in order to investigate the mechanism by which twitch force changes following an alteration of muscle length.2. A step increase in length of the muscle produced a rapid potentiation of twitch force but not of the Ca2+ transient. The rapid rise of force was unaffected by inhibiting the sarcoplasmic reticulum (SR) with ryanodine and cyclopiazonic acid.3. The force-[Ca2+](i) relationship of the myofibrils in situ, determined from twitches and tetanic contractions in SR-inhibited muscles, showed that the rapid rise of force was due primarily to an increase in myofibrillar Ca2+ sensitivity, with a contribution from an increase in the maximum force production of the myofibrils.4. After stretch of the muscle there was a further, slow increase of twitch force which was due entirely to a slow increase of the Ca2+ transient, since there was no change in the myofibrillar force-[Ca2+](i) relationship. SR inhibition slowed down, but did not alter the magnitude of, the slow force response.5. During the slow rise of force there was no slow increase of diastolic [Ca2+](i), whether or not the SR was inhibited. The same was true in unstimulated muscles.6. We conclude that the rapid increase in twitch force after muscle stretch is due to the length-dependent properties of the myofibrils. The slow force increase is not explained by length dependence of the myofibrils or the SR, or by a rise in diastolic [Ca2+](i). Evidence from tetani suggests the slow force responses result from increased Ca2+ loading of the cell during the action potential.