Ishii K, Ito K M, Ikeda M, Uemura D, Ito K
Department of Veterinary Pharmacology, Faculty of Agriculture, Miyazaki University, Japan.
Life Sci. 1997;60(7):PL91-7. doi: 10.1016/s0024-3205(96)00682-0.
Palytoxin induced increases in cytosolic Ca2+ and tension, which were dependent on external Ca2+, and depolarized the membrane in endothelium-denuded porcine coronary arteries. When the endothelium was present, however, these effects were greatly inhibited, suggesting that some factors from endothelium inhibited the palytoxin-actions. Pretreatment with 100 microM N omega-nitro-L-arginine partially reversed the inhibitory effect of endothelium on the Ca2+ movement and the contraction but not that on the depolarization. Pretreatment with 10 microM indomethacin did not affect the inhibition. These results suggest that palytoxin released both nitric oxide and endothelium-derived hyperpolarizing factor (EDHF) from the endothelium, both of which counteracted the actions of palytoxin on smooth muscle cells. It is thought that the palytoxin-induced depolarization was attenuated by hyperpolarization due to EDHF.
刺尾鱼毒素可使胞质Ca2+浓度升高并增强张力，这依赖于细胞外Ca2+，且能使去内皮猪冠状动脉的膜发生去极化。然而，当内皮存在时，这些效应受到极大抑制，提示内皮释放的某些因子可抑制刺尾鱼毒素的作用。用100微摩尔/升的Nω-硝基-L-精氨酸预处理可部分逆转内皮对Ca2+移动和收缩的抑制作用，但对去极化的抑制作用无影响。用10微摩尔/升的吲哚美辛预处理不影响这种抑制作用。这些结果表明，刺尾鱼毒素可从内皮释放一氧化氮和内皮源性超极化因子（EDHF），二者均可抵消刺尾鱼毒素对平滑肌细胞的作用。据认为，EDHF引起的超极化减弱了刺尾鱼毒素诱导的去极化。
