Case D B, Wallace J M, Keim H J, Weber M A, Sealey J E, Laragh J H
N Engl J Med. 1977 Mar 24;296(12):641-6. doi: 10.1056/NEJM197703242961201.
To block renin activity, a nonapeptide converting-enzyme inhibitor was given to 65 seated hypertensive patients. Depressor responses occurred only when control plasma renin activity exceeded 2 ng of angiotensin I per milliliter per hour and correlated directly in amplitude with control plasma renin activity and with induced increments in activity (P less than 0.001 for both). Depressor responses, like renin activity, were characteristic for renin subgroups as defined by renin-sodium profiling. Before and after sodium deprivation, the nonapeptide reduced diastolic pressure in all patients with high renin (by 17.3 and 19.8 per cent) and most patients with normal renin (by 9.1 and 17.7 per cent). Low-renin patients remained unresponsive. This enzyme blockade may cause bradykinin accumulation. But if, as seems likely, depressor responses are due to blockade of angiotensin II formation, the results indicate that, irrespective of sodium balance, measurements of plasma renin activity reflect its contribution to blood-pressure maintenance. The results suggest broad participation of the renin system in common forms of hypertension.
为阻断肾素活性，对65名坐位高血压患者给予一种九肽转化酶抑制剂。仅当对照血浆肾素活性超过每小时每毫升2纳克血管紧张素I时才出现降压反应，且降压反应的幅度与对照血浆肾素活性以及诱导的活性增量直接相关（两者的P均小于0.001）。如肾素 - 钠谱分析所定义，降压反应与肾素亚组的肾素活性一样具有特征性。在限钠前后，该九肽使所有高肾素患者的舒张压降低（分别降低17.3%和19.8%），使大多数正常肾素患者的舒张压降低（分别降低9.1%和17.7%）。低肾素患者无反应。这种酶阻断可能导致缓激肽蓄积。但如果降压反应很可能是由于血管紧张素II生成受阻所致，那么结果表明，无论钠平衡如何，血浆肾素活性的测定反映了其对血压维持的作用。结果提示肾素系统广泛参与常见类型的高血压。
