Rosenthal T, Holtzman E, Yaron A
Clin Exp Hypertens A. 1982;4(3):367-77. doi: 10.3109/10641968209060749.
The blood pressure and serum angiotensin-I converting enzyme (SACE) activity were measured in captopril-treated hypertensive patients at frequent intervals. Inhibition of SACE was observed in patients responding to the treatment with lowering of blood pressure as well as in nonresponding cases. It was therefore concluded that a mechanism not depending on the formation of angiotensin-II by ACE is responsible for the high blood pressure persisting in the captopril treated nonresponding hypertensive patients. SACE activity in sera of captopril-treated patients recovers from inhibition when stored in frozen state at -20 degrees c. An apparent dissociation was therefore observed when regeneration of SACE activity during storage of sera was not taken into account. Meaningful activities are therefore obtained only if the assay is performed without prolonged storage.
对接受卡托普利治疗的高血压患者频繁测量血压和血清血管紧张素-I转换酶（SACE）活性。在血压降低的治疗反应者以及无反应者中均观察到SACE受到抑制。因此得出结论，在接受卡托普利治疗但无反应的高血压患者中，导致高血压持续存在的机制不依赖于ACE生成血管紧张素-II。卡托普利治疗患者血清中的SACE活性在-20℃冷冻保存时会从抑制状态恢复。因此，当未考虑血清储存期间SACE活性的再生时，就会观察到明显的解离现象。因此，只有在不进行长时间储存的情况下进行测定，才能获得有意义的活性数据。
