Wright G L, Battistella-Patterson A S
Department of Physiology, Marshall University School of Medicine, Huntington, WV 25704, USA.
J Muscle Res Cell Motil. 1998 May;19(4):405-14. doi: 10.1023/a:1005301821628.
Rat aortic smooth muscle exhibits a remarkable capacity for stress relaxation, the release of tension following tissue stretch. Stress relaxation was markedly enhanced in contracted aortic rings compared with unstimulated tissue. The magnitude of stress relaxation in contracted aortic rings correlated well with the passive tension imposed on the tissue by stretching, but showed little relationship to changes in tissue length or to the level of tension developed in response to agonist stimulation prior to stretch. The enhancement of stress relaxation in precontracted tissue was not affected by intimal rubbing or treatment with L-NAME. By comparison, the removal of extracellular calcium markedly attenuated stress relaxation. In addition, the use of cytochalasin B to block actin polymerization inhibited stress relaxation, whereas colchicine, a drug used to cause microtubule disassembly, had no effect on the phenomenon. The results indicate that the enhanced stress relaxation in contracted tissue is a calcium-dependent process and is not due to passive tissue elastic properties. We suggest that stress relaxation may not involve cross-bridge formation but could be explained by the remodelling of a portion of the tension-bearing actin cytoskeleton.
大鼠主动脉平滑肌表现出显著的应力松弛能力,即组织拉伸后张力的释放。与未受刺激的组织相比,收缩的主动脉环中的应力松弛明显增强。收缩的主动脉环中的应力松弛程度与拉伸对组织施加的被动张力密切相关,但与组织长度的变化或拉伸前对激动剂刺激产生的张力水平关系不大。预收缩组织中应力松弛的增强不受内膜摩擦或L-NAME处理的影响。相比之下,去除细胞外钙显著减弱了应力松弛。此外,使用细胞松弛素B阻断肌动蛋白聚合可抑制应力松弛,而用于导致微管解聚的药物秋水仙碱对该现象没有影响。结果表明,收缩组织中增强的应力松弛是一个钙依赖过程,并非由于被动的组织弹性特性。我们认为,应力松弛可能不涉及横桥形成,但可以用一部分承载张力的肌动蛋白细胞骨架的重塑来解释。