血管内皮细胞和平滑肌细胞的血管紧张素II形成活性。

Artery Pub Date : 1993-01-01
M Ideishi, K Noda, M Sasaguri, M Ikeda, K Arakawa
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引用次数: 0

摘要

为了阐明血管内皮细胞(VEC)和平滑肌细胞(VSMC)在血管紧张素(Ang) II生成中的作用,我们使用合成Ang I和三肽肾素底物(13RS)测量了这些细胞在培养中Ang II形成的活性。血管紧张素转换酶(ACE)活性在两种类型的细胞中均被证实,并且Ang I转换活性对ACE抑制剂高度敏感。VEC和VSMC均能独立于ACE和肾素产生13RS中的Ang II。凝乳抑素部分抑制其活性。认为通过VEC和VSMC不仅可以将Ang I转化为Ang II。VEC和VSMC都具有独立于ACE和肾素的不同的Ang II形成途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Angiotensin II forming activity of vascular endothelial and smooth muscle cells.

To clarify the role of vascular endothelial cells (VEC) and smooth muscle cells (VSMC) in the generation of angiotensin (Ang) II, we measured the Ang II forming activity of these cells in culture using synthetic Ang I and tridecapeptide renin substrate (13RS). Angiotensin converting enzyme (ACE) activity was demonstrated in both types of cells, and the Ang I converting activity was highly sensitive to an ACE inhibitor. Both VEC and VSMC were able to generate Ang II from 13RS independently of ACE and renin. The activity was partially inhibited by chymostatin. It is suggested that Ang I could be converted to Ang II not only by VEC but also by VSMC. Both VEC and VSMC possess alternate Ang II forming pathways independent of ACE and renin.

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