Rasmussen S, Leth A, Ibsen H, Damkjaer Nielsen M, Nielsen F, Giese J
Acta Med Scand. 1985;218(5):435-42. doi: 10.1111/j.0954-6820.1985.tb08871.x.
The acute effects of 25 mg captopril on blood pressure, heart rate, components of the renin-angiotensin system and blood concentration of bradykinin were followed in a single-blind placebo study of untreated (group A, n = 15) and thiazide-treated (group B, n = 13) patients with mild or moderate essential hypertension. A drug-related fall in blood pressure was seen in both groups. The blood pressure reduction was more marked in group B than in group A. Heart rate remained unchanged. Plasma concentrations of angiotensin II decreased significantly with concurrent increases in plasma concentrations of renin and angiotensin I, indicating the in vivo inhibition of converting enzyme. Blood concentrations of bradykinin showed no systemic changes. The magnitude of blood pressure reduction was correlated both with the pretreatment levels and the concurrent decreases in plasma angiotensin II. Inhibition of angiotensin II formation can explain a large part of the acute hypotensive pharmacological action of captopril. Other vasoactive systems may be involved. The kallikrein-kinin system does not appear to participate as indicated by the unchanged concentrations of kinin in blood.
在一项针对未经治疗（A组，n = 15）和接受噻嗪类药物治疗（B组，n = 13）的轻度或中度原发性高血压患者的单盲安慰剂研究中，观察了25毫克卡托普利对血压、心率、肾素 - 血管紧张素系统成分以及缓激肽血药浓度的急性影响。两组均出现了与药物相关的血压下降。B组的血压降低比A组更显著。心率保持不变。血管紧张素II的血浆浓度显著降低，同时肾素和血管紧张素I的血浆浓度升高，表明体内转化酶受到抑制。缓激肽的血药浓度未显示出全身性变化。血压降低的幅度与治疗前水平以及血浆血管紧张素II的同时降低均相关。血管紧张素II形成的抑制可以解释卡托普利急性降压药理作用的很大一部分。其他血管活性系统可能也参与其中。如血液中激肽浓度未变所示，激肽释放酶 - 激肽系统似乎未参与其中。
