Crankshaw D J, Janis R A, Daniel E E
Can J Physiol Pharmacol. 1977 Oct;55(5):1028-32. doi: 10.1139/y77-141.
Several agents which antagonize or interact with Ca2+ in the excitation-contraction coupling of smooth muscle have been tested for their effects on Ca2+ accumulation by subcellular fractions of the rat uterus. Na+, but not K+, reduced the amount of Ca2+ that could be accumulated by the plasma membrane fraction (PM) and the endoplasmic reticular fraction (ER). Sr2+ considerably reduced Ca2+ accumulation by PM, ER, and the mitochondrial fraction; Ba2+ had a similar effect but was not as potent as Sr2+. La3+ at concentrations up to 10 mM was unable to block Ca2+ accumulation by PM and ER completely. The pharmacological agents D600, verapamil, and chlorpromazine all inhibited Ca+ accumulation at dose levels much higher than those required to inhibit contractility, and were ineffective at lower doses. The action of Ca2+ antagonists is seen to be complex, involving interactions at different sites and on different processes. For a fuller understanding of their mechanisms of action further studies upon passive binding and on the release of Ca2+ from subcellular sites are required.
几种在平滑肌兴奋 - 收缩偶联中与Ca2+拮抗或相互作用的药物，已针对其对大鼠子宫亚细胞组分积累Ca2+的影响进行了测试。Na+而非K+减少了质膜组分（PM）和内质网组分（ER）可积累的Ca2+量。Sr2+显著减少了PM、ER和线粒体组分对Ca2+的积累；Ba2+有类似作用，但不如Sr2+有效。浓度高达10 mM的La3+无法完全阻断PM和ER对Ca2+的积累。药理剂D600、维拉帕米和氯丙嗪均在远高于抑制收缩所需的剂量水平抑制Ca+积累，而在较低剂量时无效。可见Ca2+拮抗剂的作用很复杂，涉及在不同位点和不同过程中的相互作用。为更全面了解其作用机制，需要对被动结合以及亚细胞位点Ca2+的释放进行进一步研究。
