Prostaglandin E2 (PGE2) induced a dose-dependent increase in tone of the circular muscles of guinea pig ileum in vitro. These actions of PGE2 were deleted in the cold-stored preparations and blocked by tetrodotoxin. Atropine reduced the effects of PGE2 and physostigmine potentiated the PGE2-induced contractions. The release of acetylcholine (ACh) by PGE2 was responsible for initiating this contraction. The effect of PGE2 was compared with that of an electrical stimulation which also initiated a non-receptor-mediated release of ACh. Hexamethonium abolished the effect of PGE2 but did not influence the actions of the electrical stimulations. Synaptosomal fractions of the circular muscles were prepared to study the release of [14C]ACh. However, PGE2 failed to evoke a marked increase in the efflux of radioactivity, even at the maximal concentration. Damage and/or removal of the myenteric plexus may be responsible for this result because electrical stimulations that exert a powerful spasmogenic effect on longitudinal muscles also induced an insensitive response. Alloxan and ethacrynic acid, inhibitors of adenylate cyclase, reduced the activity of PGE2 at a concentration insufficient to modify either the actions of ACh or the electrical stimulations. 3-Isobutyl-1-methylxanthine (IBMX) potentiated the responses to PGE2 at a dose sufficient to block the activity of phosphodiesterase (PDE). Imidazole, a stimulator of PDE, decreased the actions of PGE2 in a dose-dependent manner. IBMX, like imidazole, failed to modify the activities of both ACh and the electrical stimulations. These results indicate that PGE2 may function as a releaser of ACh in a cyclic AMP-dependent manner in the circular muscles of guinea pig ileum.

译文

前列腺素E2 (PGE2) 在体外诱导豚鼠回肠环形肌张力的剂量依赖性增加。PGE2的这些作用在冷藏制剂中被删除,并被河豚毒素阻断。阿托品降低了PGE2的作用,毒扁豆碱增强了PGE2-induced收缩。PGE2释放乙酰胆碱 (ACh) 是引发这种收缩的原因。将PGE2的作用与电刺激的作用进行了比较,电刺激也启动了非受体介导的ACh释放。六甲铵消除了PGE2的作用,但不影响电刺激的作用。环状肌肉的突触体部分准备研究 [14C]ACh的释放。然而,PGE2未能引起放射性外排的显着增加,即使在最大浓度下。肌间神经丛的损伤和/或去除可能是造成这一结果的原因,因为对纵向肌肉产生强大痉挛作用的电刺激也会引起不敏感的反应。四氧嘧啶和乙酸,腺苷酸环化酶的抑制剂,降低了PGE2的活性,其浓度不足以改变ACh或电刺激的作用。3-异丁基-1-甲基黄嘌呤 (IBMX) 以足以阻断磷酸二酯酶 (PDE) 活性的剂量增强了对PGE2的反应。咪唑,PDE的刺激剂,以剂量依赖的方式降低了PGE2的作用。像咪唑一样,IBMX未能改变ACh和电刺激的活性。这些结果表明PGE2可能以循环AMP依赖的方式在豚鼠回肠的环形肌肉中起到ACh的释放作用。

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