Nakai K, Syoh T, Hiramori K
Second Department of Internal Medicine, Iwate Medical University.
Nihon Rinsho. 1995 May;53(5):1232-6.
Angiotensin I-converting enzyme (ACE) converts the largely inactive decapeptide angiotensin I to the active octapeptide angiotensin II. ACE is a key component of the renin-angiotensin system that has long been suspected to play a role in the pathogenesis of hypertension and cardiovascular disease. The ACE gene spans 21 kilobases and consists of 26 exons, and two different mRNAs and endothelial and testicular ACE are transcribed from the ACE gene. Circulating ACE probably originates from proteolytic cleavage of the hydrophobic anchor and passive leakage of the membrane-bound enzyme. Normal serum ACE by spectrophotometric assay is very low (8.3-21.4 microliters/ml). The abnormally elevated ACE levels is indeed a diagnostic aid in sarcoidosis. The ACE gene has 287 base pair insertion/deletion polymorphism in intron 16. The ACE deletion polymorphism appears to be associated with increased risk for myocardial infarction in the Caucasian and Japanese population. Recently in multicenter clinical trials (SAVE), administration of inhibitors of ACE were shown to decrease cardiac events after myocardial infarction.
血管紧张素I转换酶（ACE）可将基本无活性的十肽血管紧张素I转化为活性八肽血管紧张素II。ACE是肾素-血管紧张素系统的关键组成部分，长期以来一直被怀疑在高血压和心血管疾病的发病机制中起作用。ACE基因跨度为21千碱基，由26个外显子组成，从ACE基因转录出两种不同的mRNA以及内皮型和睾丸型ACE。循环中的ACE可能源于疏水锚定物的蛋白水解切割以及膜结合酶的被动渗漏。通过分光光度法测定，正常血清ACE水平非常低（8.3 - 21.4微升/毫升）。ACE水平异常升高确实有助于结节病的诊断。ACE基因在第16内含子中有287个碱基对的插入/缺失多态性。ACE缺失多态性似乎与白种人和日本人群中心肌梗死风险增加有关。最近在多中心临床试验（SAVE）中，ACE抑制剂的给药显示可减少心肌梗死后的心脏事件。
