Characterization of angiotensin receptors mediating prostaglandin synthesis in C6 glioma cells.
Characterization of angiotensin receptors mediating prostaglandin synthesis in C6 glioma cells.
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C6 神经胶质瘤细胞中介导前列腺素合成的血管紧张素受体的表征。
DOI：
10.1152/ajpregu.1991.260.5.r1000
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Ferrario,CM
中科院分区：
文献类型：
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作者：
Jaiswal,N;Diz,DI;Tallant,EA;Khosla,MC;Ferrario,CM
七肽血管紧张素 (ANG)-(1-7) 模仿 ANG II 的一些但不是全部的核心作用，表明可能存在受体亚型。在神经来源的大鼠 C6 神经胶质瘤细胞中研究了 ANG-(1-7)、ANG II 和 ANG I 对前列腺素 (PG) E2 和前列环素 (PGI2) 合成的影响。所有三种 ANG 肽均以剂量依赖性方式刺激 PG 释放，其效力顺序为 ANG-(1-7) 大于 ANG I 大于 ANG II。 ANG-(1-7) (10(-7) M) 诱导的 PGE2 释放被 [Sar1,Ile8]ANG II (10(-6) M)、[Sar1,Thr8]ANG II (10(-6) M) 或 1 亚型选择性拮抗剂 Du Pont 753 (10(-5) M) 部分阻断，但不被 2 亚型选择性拮抗剂 CGP 42112A 阻断(10(-7)-10(-5) M)。 PGI2 释放仅受 [Sar1,Thr8]ANG II 抑制。 ANG II 诱导的 PGE2 释放可被 [Sar1,Thr8]ANG II (10(-6) M)、[Sar1,Ile8]ANG II (10(-6) M) 或 Du Pont 753 (10(-7) M) 阻断，但不能被 CGP 42112A (10(-7)-10(-5) M) 阻断。相反，ANG II 诱导的 PGI2 释放被 Du Pont 753 (10(-7) M) 以及 [Sar1,Ile8]ANG II (10(-6) M) 阻断，但不被 [Sar1,Thr8]ANG II 或 CGP 42112A 阻断。因此，C6 神经胶质瘤细胞中 ANG II 刺激的 PGE2 和 PGI2 合成是通过受体亚型 1 介导的。ANG-(1-7) 诱导的 PGE2 合成也是通过亚型 1 受体介导的；然而，PGI2 的释放仅被 [Sar1,Thr8]ANG II 阻止。（摘要截断为 250 字）
The heptapeptide angiotensin (ANG)-(1-7) mimics some but not all the central actions of ANG II, suggesting that receptor subtypes may exist. The effects of ANG-(1-7), ANG II, and ANG I on prostaglandin (PG) E2 and prostacyclin (PGI2) synthesis were investigated in neurally derived rat C6 glioma cells. All three ANG peptides stimulated PG release in a dose-dependent manner with the order of potency ANG-(1-7) greater than ANG I greater than ANG II. PGE2 release induced by ANG-(1-7) (10(-7) M) was partially blocked by [Sar1,Ile8]ANG II (10(-6) M), [Sar1,Thr8]ANG II (10(-6) M), or the subtype 1 selective antagonist Du Pont 753 (10(-5) M) but not by the subtype 2 selective antagonist CGP 42112A (10(-7)-10(-5) M). PGI2 release was inhibited only by [Sar1,Thr8]ANG II. ANG II-induced PGE2 release was blocked by [Sar1,Thr8]ANG II (10(-6) M), [Sar1,Ile8]ANG II (10(-6) M), or Du Pont 753 (10(-7) M) but not by CGP 42112A (10(-7)-10(-5) M). In contrast, ANG II-induced PGI2 release was blocked by Du Pont 753 (10(-7) M) as well as [Sar1,Ile8]ANG II (10(-6) M) but not by [Sar1,Thr8]ANG II or CGP 42112A. Thus ANG II-stimulated PGE2 and PGI2 syntheses in C6 glioma cells are mediated via receptor subtype 1. ANG-(1-7)-induced PGE2 synthesis is also mediated via subtype 1 receptors; however, PGI2 release was blocked by [Sar1,Thr8]ANG II only.(ABSTRACT TRUNCATED AT 250 WORDS)