Gaion R M, Trento M
Br J Pharmacol. 1983 Oct;80(2):279-86. doi: 10.1111/j.1476-5381.1983.tb10031.x.
The mechanism of action of prostacyclin (PGI2) on isolated segments of guinea-pig terminal ileum was studied by recording the changes in isometric tension. In these preparations PGI2 (1 nM-1 microM) caused a concentration-dependent increase in muscle tension. This effect was rapid and short-lasting. PGI2-induced contractions were inhibited by atropine and potentiated by physostigmine. Hemicholinium-3 reduced the response to PGI2 and the inhibition was quantitatively comparable at any PGI2 concentration tested. Tetrodotoxin as well as low temperature (20 degrees C) abolished and beta-bungarotoxin reduced the effect of PGI2. Hexamethonium decreased the response to submaximal, but not to maximal PGI2 concentrations. PGI2 potentiated the twitch response of the ileum to electrical stimulation. In the presence of tetrodotoxin, PGI2 did not alter the effect of a sub-maximal concentration of acetylcholine (ACh). The present results give indirect evidence for the ability of PGI2 to facilitate ACh release from intramural nerves possibly by increasing the excitability of cholinergic cell bodies.
通过记录等长张力的变化，研究了前列环素（PGI2）对豚鼠回肠离体肠段的作用机制。在这些标本中，PGI2（1 nM - 1 μM）引起肌肉张力呈浓度依赖性增加。这种作用迅速且持续时间短。PGI2诱导的收缩被阿托品抑制，被毒扁豆碱增强。半胱氨酸3降低了对PGI2的反应，且在任何测试的PGI2浓度下，这种抑制在数量上都是可比的。河豚毒素以及低温（20℃）消除了PGI2的作用，β-银环蛇毒素降低了PGI2的作用。六甲铵降低了对次最大但不是最大PGI2浓度的反应。PGI2增强了回肠对电刺激的抽搐反应。在存在河豚毒素的情况下，PGI2没有改变次最大浓度乙酰胆碱（ACh）的作用。目前的结果间接证明了PGI2可能通过增加胆碱能细胞体的兴奋性来促进ACh从壁内神经释放的能力。
