岩沙海葵毒素对豚鼠结肠带收缩反应及钙转运的影响。

Effects of palytoxin on contractile response and calcium movement in guinea-pig taenia coli.

作者信息

Ozaki H, Nagase H, Karaki H, Urakawa N

出版信息

Comp Biochem Physiol C Comp Pharmacol Toxicol. 1987;86(2):387-93. doi: 10.1016/0742-8413(87)90101-0.

Abstract

PTX (10(-8)M) induced a rapid increase followed by a gradual decrease in muscle tension in normal physiological salt solution (PSS), while it induced a slow increase in muscle tension in low-Na+ solution. These contractions were inhibited by Ca2+ channel blockers, verapamil and nicardipine. PTX rapidly increased tissue Na+ and decreased tissue K+ contents in normal PSS. In low-Na+ solution, PTX decreased tissue K+ content with a slower rate than that in normal PSS. PTX increased uptake of 45Ca2+ in normal as well as low-Na+ solutions with similar time course as the increase in muscle tension. However, 45Ca2+ uptake still remained high when the PTX-induced transient contraction ceased. These results suggest that PTX increases Ca2+ influx through voltage-dependent Ca2+ channels to cause contraction. After a prolonged exposure to PTX, however, muscle tension is uncoupled from Ca2+ influx.

摘要

在正常生理盐溶液（PSS）中，百日咳毒素（PTX，10⁻⁸M）可引起肌肉张力迅速升高，随后逐渐下降，而在低钠溶液中，它可使肌肉张力缓慢升高。这些收缩可被钙通道阻滞剂维拉帕米和尼卡地平抑制。在正常PSS中，PTX可使组织钠含量迅速升高，钾含量降低。在低钠溶液中，PTX降低组织钾含量的速度比在正常PSS中慢。在正常和低钠溶液中，PTX均增加⁴⁵Ca²⁺的摄取，其时间进程与肌肉张力升高相似。然而，当PTX诱导的短暂收缩停止时，⁴⁵Ca²⁺摄取仍保持在较高水平。这些结果表明，PTX通过电压依赖性钙通道增加钙内流，从而引起收缩。然而，在长时间暴露于PTX后，肌肉张力与钙内流解偶联。