前列腺素类EP (1)——TP-receptors参与人类肺血管的收缩。

文章的细节

引用

复制到剪贴板

Walch L, de Montpreville V C,边缘Norel X

前列腺素类EP (1)——TP-receptors参与人类肺血管的收缩。

Br J杂志。2001年12月,134 (8):1671 - 8。

PubMed ID

11739243 (在PubMed

]

文摘

1。的前列腺素类受体(TP、FP EP(1)和/或EP(3))参与人类肺静脉的血管收缩,孤立的静脉制剂与不同的挑战prostanoid-receptor受体激动剂在没有或选择性拮抗剂的存在。2。稳定的凝血恶烷(2)模拟,U46619,是一个强有力的括约肌受体激动剂对人类肺静脉(压电陶瓷(50)= 8.60 + / - -0.11和E (max) = 4.61 + / - -0.46 g;n = 15)。的亲和力值两个选择性TP-antagonists(湾u3405和GR32191B)与U46619湾u3405: pA (2) = 8.94 + / - -0.23 (n = 3)和GR32191B:明显的pK (B) = 8.25 + / - -0.34 (n = 3),分别。这些结果符合参与的TP-receptor U46619诱导宫缩。3所示。两EP / EP(1) -(3) -受体激动剂(17-phenyl-PGE(2)和sulprostone)诱导人类pumonary静脉收缩(压电陶瓷(50)= 8.56 + / - -0.18;E (max) = 0.56 + / - -0.24克; n=5 and pEC(50)=7.65+/-0.13; E(max)=1.10+/-0.12 g; n=14, respectively). The potency ranking for these agonists: 17-phenyl-PGE(2) > sulprostone suggests the involvement of an EP(1)-receptor rather than EP(3). In addition, the contractions induced by sulprostone, 17-phenyl-PGE(2) and the IP-/EP(1)- agonist (iloprost) were blocked by the DP-/EP(1)-/EP(2)-receptor antagonist (AH6809) as well as by the EP(1) antagonist (SC19220). 4. PGF(2alpha) induced small contractions which were blocked by AH6809 while fluprostenol was ineffective. These results indicate that FP-receptors are not implicated in the contraction of human pulmonary veins. 5. These data suggest that the contractions induced by prostanoids involved TP- and EP(1)-receptors in human pulmonary venous smooth muscle.

beplay体育安全吗DrugBank数据引用了这篇文章

药物靶点

药物	目标	类	生物	药理作用	行动
Iloprost	前列腺素E2受体EP1亚型	蛋白质	人类	是的	受体激动剂	细节