Muramatsu I, Fujiwara M, Ikushima S, Ashida K
Naunyn Schmiedebergs Arch Pharmacol. 1980 Jun;312(2):193-7. doi: 10.1007/BF00569730.
Effects of a marine polypeptide, Goniopora toxin (GPT) (molecular weight 12,000), were examined in isolated blood vessels guinea pigs. GPT, ranging from 10-100 nM, augmented the contractile response to electrical transmural stimulation in the thoracic aorta, portal vein, and mesenteric and femoral arteries. The effects were abolished by tetrodotoxin and bretylium, and were markedly attenuated by phentolamine. As GTP did not affect the resting tension spontaneous rhythmicity or noradrenaline-induced contraction, the toxin appears to act on the neural elements in the vascular wall rather than on the smooth muscle. In the portal vein preloaded with 3H-noradrenaline, GPT enhanced the 3H-efflux in response to electrical transmural stimulation, yet had not effect on the spontaneous efflux. The increase in stimulation-evoked 3H-efflux caused by GPT was more than 15 times larger than the increase seen with cocaine or phentolamine. Tetrodotoxin completely blocked the 3H-efflux induced by electrical transmural stimulation. These data suggest that GPT acts on nerve components in guinea pig blood vessels and increases the release of noradrenaline evoked by electrical stimulation of the nerve fibers. These effects are probably associated with prolongation of the action potential duration and repetitive discharges in the adrenergic nerve fibers.
在豚鼠离体血管中研究了一种海洋多肽——角珊瑚毒素（GPT，分子量12,000）的作用。GPT浓度在10 - 100 nM之间时，可增强胸主动脉、门静脉、肠系膜动脉和股动脉对经壁电刺激的收缩反应。河豚毒素和溴苄胺可消除这些作用，酚妥拉明可使其明显减弱。由于GPT不影响静息张力、自发节律性或去甲肾上腺素诱导的收缩，该毒素似乎作用于血管壁中的神经成分而非平滑肌。在预先加载3H - 去甲肾上腺素的门静脉中，GPT可增强经壁电刺激引起的3H - 流出，但对自发流出无影响。GPT引起的刺激诱发3H - 流出增加比可卡因或酚妥拉明引起的增加大15倍以上。河豚毒素完全阻断了经壁电刺激诱导的3H - 流出。这些数据表明，GPT作用于豚鼠血管中的神经成分，并增加电刺激神经纤维诱发的去甲肾上腺素释放。这些作用可能与肾上腺素能神经纤维动作电位持续时间的延长和重复放电有关。
