Ohman K P, Karlberg B E, Nilsson O R, Wettre S
Acta Med Scand Suppl. 1981;646:98-105.
The effects of captopril (SQ 14.225), an orally active inhibitor of angiotensin converting enzyme, were investigated in a dose titration study of primary hypertension. In 32 patients 4 weeks titration with captopril gave a mean blood pressure (BP) reduction of 26/16 mmHg supine and 30/16 mmHg standing. No serious side effects were observed. The BP lowering effect was related to pretreatment plasma renin activity and was less in low renin hypertension (p less than 0.05). Captopril reduced angiotensin II (p less than 0.05), plasma (p less than 0.005) and urinary aldosterone (p less than 0.001) as well as urinary kallikrein excretion (p less than 0.005). Captopril (SQ 14.225) is a competitive inhibitor of peptidyl dipeptide hydrolase, also known as angiotensin converting enzyme (ACE) or kininase II, which converts angiotensin I (A I) into angiotensin II (A II), hydrolyzes des-Asp-angiotensin I to angiotensin III (A III) and inactivates bradykinin (BK) (19). Captopril has potent antihypertensive effects when used in human hypertension (review, 3) especially when the renin-angiotensin-aldosterone system (RAAS) is activated. To further investigate the mode of action and the hypotensive effect of captopril, we measured plasma renin activity (PRA), A II, plasma (PA) and urinary aldosterone excretion (UA) and urinary kallikrein excretion (UK) in 32 patients with established primary (essential) hypertension.
在一项原发性高血压剂量滴定研究中，对口服活性血管紧张素转换酶抑制剂卡托普利（SQ 14.225）的效果进行了研究。在32例患者中，用卡托普利进行4周滴定后，仰卧位平均血压（BP）降低26/16 mmHg，站立位降低30/16 mmHg。未观察到严重副作用。血压降低效果与治疗前血浆肾素活性有关，在低肾素性高血压患者中效果较差（p<0.05）。卡托普利降低了血管紧张素II（p<0.05）、血浆（p<0.005）和尿醛固酮（p<0.001）以及尿激肽释放酶排泄（p<0.005）。卡托普利（SQ 14.225）是肽基二肽水解酶的竞争性抑制剂，该酶也称为血管紧张素转换酶（ACE）或激肽酶II，它将血管紧张素I（AI）转化为血管紧张素II（AII），将去天冬氨酸血管紧张素I水解为血管紧张素III（AIII）并使缓激肽（BK）失活（19）。卡托普利用于人类高血压时具有强大的降压作用（综述，3），尤其是在肾素-血管紧张素-醛固酮系统（RAAS）被激活时。为了进一步研究卡托普利的作用方式和降压效果，我们测量了32例确诊的原发性（特发性）高血压患者的血浆肾素活性（PRA）、AII、血浆（PA）和尿醛固酮排泄（UA）以及尿激肽释放酶排泄（UK）。
