Fletcher J E, Tripolitis L, Beech J
Department of Anesthesiology, Hahnemann University, Philadelphia, PA 19102.
Life Sci. 1992;51(22):1731-8. doi: 10.1016/0024-3205(92)90302-6.
The modulation of Ca2+ release by synthetic bee venom melittin was examined in equine and human terminal cisternae-containing fractions. Melittin (0.1 microM) decreased the threshold of Ca(2+)-induced Ca2+ release by 20% in equine muscle and by 36% in human muscle. If terminal cisternae fractions were first preloaded with Ca2+ to greater than about 75% of the threshold of Ca(2+)-induced Ca2+ release and then melittin added, an immediate and sustained release of Ca2+ occurred in preparations from both species. Addition of melittin after a Ca2+ preload of < 50% of the threshold of Ca(2+)-induced Ca2+ release did not elicit sustained Ca2+ release. Ruthenium red (10 microM) antagonized all effects of melittin on Ca2+ release. Melittin (0.1-10 microM) did not affect [3H]ryanodine binding. Melittin (0.1 microM) slightly (10%) inhibited the Ca2+ pump and this action was not antagonized by ruthenium red. These findings suggest that melittin may be an important new probe of the Ca(2+)-modulated Ca2+ release process that does not act at the ryanodine binding site.
在含有马和人终池的组分中研究了合成蜂毒蜂毒素对Ca2+释放的调节作用。蜂毒素（0.1微摩尔）使马肌肉中Ca2+诱导的Ca2+释放阈值降低20%，使人肌肉中降低36%。如果先将终池组分预加载Ca2+至大于Ca2+诱导的Ca2+释放阈值的约75%，然后加入蜂毒素，则两种物种的制剂中都会立即出现持续的Ca2+释放。在Ca2+预加载量低于Ca2+诱导的Ca2+释放阈值的50%后加入蜂毒素，不会引发持续的Ca2+释放。钌红（10微摩尔）拮抗蜂毒素对Ca2+释放的所有作用。蜂毒素（0.1 - 10微摩尔）不影响[3H]ryanodine结合。蜂毒素（0.1微摩尔）轻微（10%）抑制Ca2+泵，且这种作用不受钌红拮抗。这些发现表明，蜂毒素可能是Ca2+调节的Ca2+释放过程的一种重要新探针，其作用位点不在ryanodine结合位点。
