前列腺素类的有力收缩动作EP3-receptor受体激动剂对人类孤立的肺动脉。

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陈黔YM,琼斯RL,公里,股票AI,何鸿燊JK

前列腺素类的有力收缩动作EP3-receptor受体激动剂对人类孤立的肺动脉。

Br J杂志。1994年10月,113 (2):369 - 74。

PubMed ID

7834185 (在PubMed

]

文摘

1。在13个15实验,前列腺素E2 (PGE2)和sulprostone(前列腺素类EP1 / EP3-receptor受体激动剂)简约孤立的人类肺动脉环在低浓度(> = 5 >或= 0.5 nM)。组织获得病人手术主要用于癌的肺。特征相关的受体被损失的敏感性复杂收缩铂族元素在实验期间的行动。相比之下,收缩反应氯化钾、去甲肾上腺素和特定的凝血恶烷(TP)受体激动剂,u - 46619,没有随时间减少。2。相对收缩效力七铂族元素的类似物,在发生后的最初数小时内设置准备,如下:sulprostone >米索前列醇= gemeprost >或= PGE2 > = GR 63799 x > 17-phenyl-omega-trinor PGE2 > = 11-deoxy PGE1。这排名表明一个EP3-receptor。3所示。sulprostone的收缩作用不被TP-receptor拮抗剂,EP 169和GR 32191, EP1-receptor拮抗剂,6809啊。 4. In two experiments, PGE2 (50 nM) reduced basal tone and sulprostone was a weak contractile agent. Phenylephrine-induced tone was also inhibited by PGE2 (EC50 = 5-20 nM), 11-deoxy PGE1 and butaprost (a selective EP2-receptor agonist); the latter prostanoids were about 2 and 4 times less potent than PGE2 respectively. Interactions with phenylephrine were different in experiments where PGE2 alone was contractile: PGE2 induced contraction superimposed on the phenylephrine response and 11-deoxy PGE1 induced either further contraction or had no effect. Butaprost produced relaxation at high concentrations;this may not be an EP2 action since preparations were highly sensitive to relaxant actions of prostacyclin (IP-) receptor agonists (cicaprost and TEI-9063).5 The study has shown that in the majority of experiments on the human isolated pulmonary artery,the contractile EP3 system outweighed the relaxant EP2 system. However, in two experiments the reverse was true. It is not clear to what extent these differences are due to disease processes affecting the tissues.The findings are discussed in relation to the adverse cardiovascular responses occasionally encountered during treatment of postpartum haemorrhage with sulprostone, and more generally to the clinical use of EP-receptor agonists in man.

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药物靶点

药物	目标	类	生物	药理作用	行动
Gemeprost	前列腺素E2受体EP3亚型	蛋白质	人类	是的	受体激动剂	细节