Dux S, Aron N, Boner G, Carmel A, Yaron A, Rosenfeld J B
Isr J Med Sci. 1984 Dec;20(12):1138-42.
The serum converting enzyme activity (SCEA) was measured in 86 healthy individuals (1.44 +/- 0.82 u, mean +/- SD), 39 patients with essential hypertension (1.53 +/- 0.71 u), 7 patients with hypertension due to renal artery stenosis (1.76 +/- 0.77 u), 14 patients with chronic renal failure (2.10 +/- 0.57 u), 7 patients with renal failure and hypertension (2.62 +/- 0.35 u), 22 normotensive pregnant women (1.02 +/- 0.26 u) and 6 hypertensive pregnant women (1.1 +/- 0.3). No difference was detected between men and women or between normotensives and hypertensives. However, a significant rise in SCEA was found in patients with chromic renal failure (P less than 0.005), in whom an enlarged pulmonary vascular bed and accelerated cellular breakdown are thought to be the causes of the elevated SCEA. During pregnancy, subnormal SCEA was found (P less than 0.005), and this is thought to be due to the enzyme consumption in the kinin system, which is activated during pregnancy. We assume that converting enzyme is not a limiting factor in angiotensin conversion, and most probably it does not contribute significantly to the pathogenesis of hypertension.
对86名健康个体（血清转换酶活性[SCEA]为1.44±0.82单位，均值±标准差）、39名原发性高血压患者（1.53±0.71单位）、7名肾动脉狭窄所致高血压患者（1.76±0.77单位）、14名慢性肾衰竭患者（2.10±0.57单位）、7名肾衰竭合并高血压患者（2.62±0.35单位）、22名血压正常的孕妇（1.02±0.26单位）以及6名高血压孕妇（1.1±0.3单位）进行了血清转换酶活性测定。未检测到男性与女性之间或血压正常者与高血压患者之间存在差异。然而，慢性肾衰竭患者的SCEA显著升高（P<0.005），据认为其肺血管床扩大和细胞分解加速是SCEA升高的原因。在孕期，发现SCEA低于正常水平（P<0.005），据认为这是由于孕期激活的激肽系统消耗了该酶所致。我们假定转换酶不是血管紧张素转换的限制因素，而且很可能它对高血压的发病机制贡献不大。
