Frank G B, Rohani F
Can J Physiol Pharmacol. 1982 Jan;60(1):47-51. doi: 10.1139/y82-006.
The effects of Ba2+ ions on twitches, K+-induced contractures, and on intracellularly recorded membrane potentials (Em) and depolarizations of frog skeletal muscle fibres were investigated. Exposure of toe muscles to choline--Ringer's solution with 10(-3) M Ba2+ with Ca2+ (1.08 mM) eliminated or very greatly reduced contractures produced by 60 mM K+. In contrast, not only did the same concentration of Ba2+ ions fail to depress the twitch tension of isolated semitendinosus fibres when added to Ringer's with Ca2+, but it even restored twitches that had been eliminated in a zero Ca2+ Ringer's solution. The resting Em of sartorius muscle fibres in choline--Ringer's solution was reduced about 20 mV by 10(-3) M Ba2+. This Ba2+ ion concentration also antagonized the K+-induced depolarization. Thus in the presence of 1 mM Ba2+, 20 mM K+ hyperpolarized rather than depolarized the fibres and 60 or 123 mM K+ produced only very slowly developing, small depolarizations. These results suggest that the loss of the K+-induced contracture in choline-Ringer's caused by Ba2+ ions is due to an inhibition of the K+-induced depolarization. The latter result is consistent with previous findings of other workers that Ba2+ ions block membrane K+ channels.
研究了Ba2+离子对青蛙骨骼肌纤维的抽搐、钾离子诱导的挛缩以及细胞内记录的膜电位（Em）和去极化的影响。将趾肌暴露于含有10(-3) M Ba2+和Ca2+（1.08 mM）的胆碱 - 林格氏溶液中，可消除或极大地降低由60 mM K+产生的挛缩。相比之下，当向含有Ca2+的林格氏溶液中添加相同浓度的Ba2+离子时，不仅不会降低离体半腱肌纤维的抽搐张力，反而能恢复在零Ca2+林格氏溶液中已消除的抽搐。在胆碱 - 林格氏溶液中，10(-3) M Ba2+使缝匠肌纤维的静息Em降低约20 mV。该Ba2+离子浓度还能拮抗钾离子诱导的去极化。因此，在存在1 mM Ba2+的情况下，20 mM K+使纤维发生超极化而非去极化，60或123 mM K+仅产生非常缓慢发展的小去极化。这些结果表明，Ba2+离子导致胆碱 - 林格氏溶液中钾离子诱导的挛缩丧失是由于抑制了钾离子诱导的去极化。后一结果与其他研究人员先前的发现一致，即Ba2+离子可阻断膜钾离子通道。
