Bagni M A, Colombini B, Geiger P, Berlinguer Palmini R, Cecchi G
Dipartimento di Scienze Fisiologiche, Università degli Studi di Firenze, 50134 Florence, Italy.
Am J Physiol Cell Physiol. 2004 Jun;286(6):C1353-7. doi: 10.1152/ajpcell.00493.2003. Epub 2004 Jan 28.
At the end of the force transient elicited by a fast stretch applied to an activated frog muscle fiber, the force settles to a steady level exceeding the isometric level preceding the stretch. We showed previously that this excess of tension, referred to as "static tension," is due to the elongation of some elastic sarcomere structure, outside the cross bridges. The stiffness of this structure, "static stiffness," increased upon stimulation following a time course well distinct from tension and roughly similar to intracellular Ca(2+) concentration. In the experiments reported here, we investigated the possible role of Ca(2+) in static stiffness by comparing static stiffness measurements in the presence of Ca(2+) release inhibitors (D600, Dantrolene, (2)H(2)O) and cross-bridge formation inhibitors [2,3-butanedione monoxime (BDM), hypertonicity]. Both series of agents inhibited tension; however, only D600, Dantrolene, and (2)H(2)O decreased at the same time static stiffness, whereas BDM and hypertonicity left static stiffness unaltered. These results indicate that Ca(2+), in addition to promoting cross-bridge formation, increases the stiffness of an (unidentified) elastic structure of the sarcomere. This stiffness increase may help in maintaining the sarcomere length uniformity under conditions of instability.
当对一条被激活的青蛙肌肉纤维施加快速拉伸所引发的力瞬变结束时，力会稳定在一个超过拉伸前等长水平的稳定水平。我们之前表明，这种额外的张力，即“静态张力”，是由于横桥之外的一些弹性肌节结构的伸长所致。这种结构的刚度，即“静态刚度”，在刺激后会增加，其时间进程与张力明显不同，且大致与细胞内Ca(2+)浓度相似。在本文报道的实验中，我们通过比较在存在Ca(2+)释放抑制剂（D600、丹曲林、(2)H(2)O）和横桥形成抑制剂[2,3-丁二酮一肟（BDM）、高渗]的情况下的静态刚度测量结果，研究了Ca(2+)在静态刚度中的可能作用。这两类试剂都抑制了张力；然而，只有D600、丹曲林和(2)H(2)O同时降低了静态刚度，而BDM和高渗对静态刚度没有影响。这些结果表明，Ca(2+)除了促进横桥形成外，还增加了肌节中一种（未确定的）弹性结构的刚度。这种刚度增加可能有助于在不稳定条件下维持肌节长度的均匀性。
