Ishida Y, Satake N, Habon J, Kitano H, Shibata S
J Pharmacol Exp Ther. 1985 Feb;232(2):557-60.
Palytoxin (PTX), C129H223O3N54, isolated from marine coelenterates of Palythoa tuberculosa, caused contraction of the human umbilical artery in a dose-dependent manner (10(-11)-10(-8) M). Pretreatment with ouabain (10(-5) M) abolished the PTX (10(-8) M)-induced contraction but had no effect on the serotonin- (10(-6) M) and potassium- (40 mM) induced contractions. When the muscle was exposed to a potassium-free medium, application of PTX was able to cause a contraction similar to the contraction in normal medium. In the presence of verapamil (3 X 10(-6) M) or in the calcium-free medium. PTX-induced contraction was inhibited. In the depolarized muscle with 126 mM potassium, PTX did not induce a contraction whereas serotonin did. Our results suggest that PTX causes calcium influx through the plasma membrane of the umbilical artery, causing contraction. The site of action of PTX is presumably related to the Na,K-ATPase on the plasma membrane, although the precise relation between the site of action and increase in calcium influx is not known now.
从多疣海葵的海洋腔肠动物中分离出的刺尾鱼毒素（PTX），化学式为C129H223O3N54，能以剂量依赖方式（10^(-11)-10^(-8)M）引起人脐动脉收缩。用哇巴因（10^(-5)M）预处理可消除PTX（10^(-8)M）诱导的收缩，但对血清素（10^(-6)M）和钾（40mM）诱导的收缩无影响。当肌肉暴露于无钾培养基时，施加PTX能够引起与正常培养基中相似的收缩。在维拉帕米（3×10^(-6)M）存在下或在无钙培养基中，PTX诱导的收缩受到抑制抑制。在含有126mM钾的去极化肌肉中，PTX不诱导收缩，而血清素能诱导收缩。我们的结果表明，PTX通过脐动脉的质膜引起钙内流，从而导致收缩。PTX的作用位点可能与质膜上的钠钾ATP酶有关，尽管目前尚不清楚作用位点与钙内流增加之间的确切关系。 抑制。
