岩沙海葵毒素对豚鼠主动脉血管平滑肌的收缩作用机制。

The mechanism of contractile action of palytoxin on vascular smooth muscle of guinea-pig aorta.

作者信息

Ozaki H, Tomono J, Nagase H, Urakawa N

出版信息

Jpn J Pharmacol. 1983 Dec;33(6):1155-62. doi: 10.1254/jjp.33.1155.

DOI:10.1254/jjp.33.1155

Abstract

The mode of action of palytoxin (PTX) on the contractile responses and ion movements in guinea-pig aorta was investigated. PTX (10(-8) M) induced a contraction with a latency period of 0.5-1 min, and it reached maximum after about 20 min. This contraction was not affected by phentolamine (10(-6) M). The contraction induced by PTX was rapidly abolished by removal of external Ca. Readdition of Ca restored the contraction. Verapamil, which markedly antagonized the contraction induced by some depolarizing agents (K, Ba and tetraethylammonium), decreased the rate of rise of the PTX-induced contraction, but did not affect the sustained tension level. Removal of external Na markedly inhibited the contraction induced by PTX (10(-10) - 10(-8) M), while it had no effect on the contraction induced by histamine (10(-7) - 10(-5) M). PTX rapidly decreased tissue K content with a similar time course to that of the increase in tension. Ouabain (10(-4) M) also caused contraction and decreased tissue K content in the muscle, but the rate of these changes was much slower than the PTX-induced ones. PTX increased cellular 45Ca content in normal solution, but not in Na deficient solution. These results suggest that the PTX-induced contraction in guinea-pig aorta is due to an increase in membrane Na permeability.

摘要

研究了刺尾鱼毒素（PTX）对豚鼠主动脉收缩反应和离子运动的作用方式。PTX（10⁻⁸ M）诱导的收缩潜伏期为0.5 - 1分钟，约20分钟后达到最大值。这种收缩不受酚妥拉明（10⁻⁶ M）影响。去除细胞外钙可迅速消除PTX诱导的收缩。重新添加钙可恢复收缩。维拉帕米能显著拮抗某些去极化剂（钾、钡和四乙铵）诱导的收缩，它降低了PTX诱导收缩的上升速率，但不影响持续张力水平。去除细胞外钠显著抑制了PTX（10⁻¹⁰ - 10⁻⁸ M）诱导的收缩，而对组胺（10⁻⁷ - 10⁻⁵ M）诱导的收缩没有影响。PTX能使组织钾含量迅速降低，其时间进程与张力增加相似。哇巴因（10⁻⁴ M）也可引起肌肉收缩并降低组织钾含量，但这些变化的速率比PTX诱导的要慢得多。在正常溶液中，PTX可增加细胞45钙含量，但在缺钠溶液中则不然。这些结果表明，PTX诱导的豚鼠主动脉收缩是由于膜钠通透性增加所致。