Adler K B, Krill J, Alberghini T V, Evans J N
Cell Motil. 1983;3(5-6):545-51. doi: 10.1002/cm.970030521.
Cylindrical segments of extraparenchymal pulmonary artery (essentially a preparation of smooth muscle with regard to contractile capability) were isolated from adult male rats. They were mounted in an isometric muscle bath in physiological salt solution (PSS) in an environment of 95% O2/5% CO2. After allowing 1 h for equilibration, the maximum force generated by the tissue in response to a depolarizing solution was determined. After relaxation, vessels were incubated for 1 h in one of several concentrations of cytochalasin D (CD) (0.01, 0.05, 0.5, 1, 10 micrograms/ml) and the response to stimulation retested immediately after returning to PSS, and then at 30 minute intervals up to 2 h. CD inhibited the ability of vascular smooth muscle to generate force (contract) in a concentration-dependent manner. The inhibitory effect was reversible within a short period of time. Quantitative electron microscopic examination of these vessels suggested that CD disrupts the integrity of myofilaments, especially at sites of "dense bodies." Our results indicate that a percentage of actin in smooth muscle cells is not permanently in the filamentous "F" form, but is part of the G:F actin system of the cell, labile to polymerization:depolymerization. The ability of smooth muscle cells to generate force could depend on the proper functioning of the F:G actin "treadmill."
从成年雄性大鼠中分离出肺实质外肺动脉的圆柱状节段（就收缩能力而言，本质上是平滑肌制剂）。将它们安装在生理盐溶液（PSS）中的等长肌槽中，置于95% O₂/5% CO₂的环境中。平衡1小时后，测定组织对去极化溶液产生的最大力。松弛后，将血管在几种浓度（0.01、0.05、0.5、1、10微克/毫升）的细胞松弛素D（CD）中孵育1小时，回到PSS后立即重新测试对刺激的反应，然后每隔30分钟测试一次，直至2小时。CD以浓度依赖性方式抑制血管平滑肌产生力（收缩）的能力。这种抑制作用在短时间内是可逆的。对这些血管进行的定量电子显微镜检查表明，CD破坏了肌丝的完整性，尤其是在“致密体”部位。我们的结果表明，平滑肌细胞中一定比例的肌动蛋白并非永久处于丝状“F”形式，而是细胞G:F肌动蛋白系统的一部分，对聚合：解聚不稳定。平滑肌细胞产生力的能力可能取决于F:G肌动蛋白“跑步机”的正常运作。
