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卡托普利在培养的人内皮细胞中诱导血管紧张素I转换酶的生成。

Induction of angiotensin I-converting enzyme by captopril in cultured human endothelial cells.

作者信息

Fyhrquist F, Hortling L, Grönhagen-Riska C

出版信息

J Clin Endocrinol Metab. 1982 Oct;55(4):783-6. doi: 10.1210/jcem-55-4-783.

Abstract

Captopril (2.0 microgram/ml) increased angiotensin-converting enzyme (ACE, kininase II) activity from 6- to 16-fold in culture medium of human endothelial cells from umbilical cord artery. Immunohistochemically detectable ACE was markedly increased in these cells when using rabbit antihuman lung ACE antiserum. This accords with either observations of increased ACE activity in serum and lungs from rats treated with captopril and shows induction of ACE biosynthesis in human vascular endothelial cells in culture. This observation offers a tool for studying the mechanism of ACE induction.

摘要

卡托普利(2.0微克/毫升)使来自脐带动脉的人内皮细胞培养基中的血管紧张素转换酶(ACE,激肽酶II)活性提高了6至16倍。当使用兔抗人肺ACE抗血清时,这些细胞中免疫组织化学可检测到的ACE明显增加。这与用卡托普利治疗的大鼠血清和肺中ACE活性增加的观察结果一致,并表明在培养的人血管内皮细胞中诱导了ACE生物合成。这一观察结果为研究ACE诱导机制提供了一个工具。

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