Lijnen P, Fagard R, Staessen J, Verschueren L J, Amery A
Eur J Clin Pharmacol. 1981;20(1):1-8. doi: 10.1007/BF00554659.
The acute hypotensive effect of captopril 25 mg was investigated in 26 hypertensive patients (11 with essential and 15 with renal arterial disease). Intra-arterial blood pressure was recorded continuously and arterial blood was sampled for renin, angiotensin I and II, aldosterone, kininase II, catecholamines and prostaglandins. Captopril led to an increase in plasma renin activity, active and total plasma renin concentration and angiotensin I, a decrease in plasma kininase II activity, angiotensin II, aldosterone, prostaglandins E2 and F2 alpha and no change in plasma (nor) adrenaline, dopamine and inactive renin concentration. The hypotensive effect of captopril was related to the changes in plasma angiotensin II level and inversely to the changes in prostaglandin E2; the correlation coefficients were low, respectively 0.61 and -0.44. It is likely that the acute hypotensive effect of captopril to some extent is related to changes in plasma angiotensin II and in prostaglandins E2 and F2 alpha. There is no evidence for a role of the adrenergic systems in the hypotensive response.
对26例高血压患者（11例原发性高血压患者和15例肾动脉疾病患者）研究了25毫克卡托普利的急性降压作用。连续记录动脉内血压，并采集动脉血样本检测肾素、血管紧张素I和II、醛固酮、激肽酶II、儿茶酚胺和前列腺素。卡托普利导致血浆肾素活性、活性和总血浆肾素浓度以及血管紧张素I增加，血浆激肽酶II活性、血管紧张素II、醛固酮、前列腺素E2和F2α降低，血浆（去甲）肾上腺素、多巴胺和无活性肾素浓度无变化。卡托普利的降压作用与血浆血管紧张素II水平的变化有关，与前列腺素E2的变化呈负相关；相关系数较低，分别为0.61和-0.44。卡托普利的急性降压作用可能在一定程度上与血浆血管紧张素II以及前列腺素E2和F2α的变化有关。没有证据表明肾上腺素能系统在降压反应中起作用。
