Evans D H, Chipouras E, Toop T, Donald J A
Department of Zoology, University of Florida, Gainesville 32611.
Toxicology. 1993 Oct 25;83(1-3):1-8. doi: 10.1016/0300-483x(93)90086-8.
We examined the effect of Ca2+, Cd2+, or Ni2+ on vascular smooth muscle intracellular proteins involved in contraction, using rings of detergent-permeabilized aortae from the spiny dogfish, Squalus acanthias. Addition of Ca2+ stimulated contraction of the vascular smooth muscle, and permeabilization by treatment with Triton X-100 increased the sensitivity to Ca2+ nearly 5 log units, demonstrating that this protocol left contractile and regulatory proteins intact. Addition of 1 microM calmodulin did not increase the sensitivity of the rings to Ca2+, suggesting that this preparation is not leaky to this regulatory protein. Neither Cd2+ nor Ni2+ stimulated contraction of permeabilized rings demonstrating that the previously-described contractile action of these heavy metals is not mediated by direct stimulation of intracellular proteins, rather by interaction with sarcolemmal proteins.
我们使用来自白斑角鲨（Squalus acanthias）的经去污剂通透处理的主动脉环，研究了Ca2+、Cd2+或Ni2+对参与收缩的血管平滑肌细胞内蛋白质的影响。添加Ca2+刺激血管平滑肌收缩，用Triton X-100处理进行通透处理可使对Ca2+的敏感性增加近5个对数单位，这表明该实验方案使收缩蛋白和调节蛋白保持完整。添加1 microM钙调蛋白并未增加环对Ca2+的敏感性，这表明该制剂对这种调节蛋白没有泄漏。Cd2+和Ni2+均未刺激通透环的收缩，这表明这些重金属先前描述的收缩作用不是由直接刺激细胞内蛋白质介导的，而是通过与肌膜蛋白相互作用介导的。
