Fryer M W, Gage P W, Neering I R, Dulhunty A F, Lamb G D
Department of Physiology and Pharmacology, University of N.S.W., Kensington, Australia.
Pflugers Arch. 1988 Jan;411(1):76-9. doi: 10.1007/BF00581649.
The chemical phosphatase butanedione monoxime (BDM) reversibly inhibited twitches and tetanic contractions in bundles of rat soleus fibres in a dose-dependent manner (2-20 mM) but had no effect on the amplitude or time course of action potentials. In addition, BDM reversibly reduced the amplitude of potassium contractures demonstrating a depressant effect on contraction not mediated by action potentials. BDM had no effect on asymmetric charge movement but depressed calcium currents across the surface membrane in voltage-clamped fibres. The most significant effect of BDM on excitation-contraction coupling was a reduction in the amplitude of the calcium transient associated with contraction in aequorin-injected fibres. While these experiments do not eliminate the possibility of a direct effect of BDM on contractile filaments, reduction of calcium release from the sarcoplasmic reticulum, at least at low concentrations of BDM (below 2 mM), would seem to be the main mechanism for the inhibition of contractions in rat skeletal muscle.
化学物质丁二酮单肟（BDM）以剂量依赖性方式（2 - 20 mM）可逆地抑制大鼠比目鱼肌纤维束的单收缩和强直收缩，但对动作电位的幅度或时程没有影响。此外，BDM可逆地降低钾离子挛缩的幅度，表明其对收缩有抑制作用，且这种抑制作用不是由动作电位介导的。BDM对不对称电荷移动没有影响，但在电压钳制的纤维中会抑制跨表面膜的钙电流。BDM对兴奋 - 收缩偶联最显著的影响是降低了注射水母发光蛋白的纤维中与收缩相关的钙瞬变幅度。虽然这些实验并未排除BDM对收缩丝有直接作用的可能性，但至少在低浓度BDM（低于2 mM）时，肌浆网钙释放的减少似乎是BDM抑制大鼠骨骼肌收缩的主要机制。
