Stimulation of endothelial cell prostaglandin production by angiotensin peptides. Characterization of receptors.
Stimulation of endothelial cell prostaglandin production by angiotensin peptides. Characterization of receptors.
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血管紧张素肽刺激内皮细胞前列腺素的产生。
DOI：
10.1161/01.hyp.19.2_suppl.ii49
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Ferrario,CM
中科院分区：
文献类型：
--
作者：
Jaiswal,N;Diz,DI;Chappell,MC;Khosla,MC;Ferrario,CM
血管紧张素II通过激活存在于内皮细胞、血管平滑肌细胞或两者中的血管紧张素受体来刺激血管中的前列腺素释放。我们评价了血管紧张素II、血管紧张素I和[des-Phe 8]血管紧张素II [血管紧张素-（1 - 7）]对猪主动脉内皮细胞前列腺素释放的反应。用血管紧张素I和血管紧张素-（1 - 7）孵育细胞单层，但不使用血管紧张素II，以剂量依赖性方式（10（-10）至10（-6）M）刺激前列腺素E2和前列腺素I2的释放，EC 50约为1 nM。此外，我们的特点是血管紧张素受体亚型介导的前列腺素合成，使用亚型选择性拮抗剂。血管紧张素I刺激的前列腺素合成不被任何非选择性经典血管紧张素受体拮抗剂[Sar 1，Thr 8]血管紧张素II或[Sar 1，Ile 8]血管紧张素II改变。相反，血管紧张素1亚型（AT 1）拮抗剂DuP 753或2亚型（AT 2）拮抗剂CGP 42112 A显著减弱了对血管紧张素I的前列腺素释放反应。然而，PD123177，另一种AT2拮抗剂，不抑制血管紧张素I刺激的前列腺素释放。血管紧张素-（1 - 7）诱导的前列腺素释放被[Sar 1，Thr 8]血管紧张素II（10（-6）M）和PD 123177（10（-6）M）显著减弱，但不被[Sar 1，Ile 8]血管紧张素II、DuP 753或CGP 42112 A减弱。较高剂量（10（-5）M）的DuP 753和CGP 42112 A减弱血管紧张素-（1 - 7）反应。这些数据表明，在猪主动脉内皮细胞，血管紧张素I和血管紧张素-（1 - 7），但不是血管紧张素II是有效的刺激前列腺素合成。（250字处删节）
Angiotensin II stimulates prostaglandin release in blood vessels via activation of angiotensin receptors present in endothelium, vascular smooth muscle cells, or both. We evaluated the response of angiotensin II, angiotensin I, and [des-Phe8] angiotensin II [angiotensin-(1-7)] on prostaglandin release in porcine aortic endothelial cells. Incubation of cell monolayers with angiotensin I and angiotensin-(1-7), but not angiotensin II, stimulated the release of prostaglandin E2 and prostaglandin I2 in a dose-dependent manner (10(-10) to 10(-6) M) with an EC50 of approximately 1 nM. In addition, we characterized the angiotensin receptor subtypes mediating prostaglandin synthesis by using subtype-selective antagonists. Angiotensin I-stimulated prostaglandin synthesis was not altered by either of the nonselective classical angiotensin receptor antagonists [Sar1,Thr8]angiotensin II or [Sar1,Ile8]angiotensin II. In contrast, either the angiotensin subtype 1 (AT1) antagonist DuP 753 or the subtype 2 (AT2) antagonist CGP42112A significantly attenuated the prostaglandin release in response to angiotensin I. However, PD123177, another AT2 antagonist, did not inhibit angiotensin I-stimulated prostaglandin release. Angiotensin-(1-7)-induced prostaglandin release was significantly attenuated by [Sar1,Thr8]angiotensin II (10(-6) M) and PD123177 (10(-6) M) but not by [Sar1,Ile8]angiotensin II, DuP 753, or CGP42112A. Higher doses (10(-5) M) of DuP 753 and CGP42112A attenuated the angiotensin-(1-7) response. These data suggest that in porcine aortic endothelial cells, angiotensin I and angiotensin-(1-7) but not angiotensin II are potent stimuli for prostaglandin synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)