Kamei H, Arakawa K
Jpn Heart J. 1982 Mar;23(2):191-9. doi: 10.1536/ihj.23.191.
An angiotensin converting enzyme inhibitory, captopril (or SQ 14225), was administered orally to 23 hypertensive patients under a constant sodium and potassium diet. It resulted in reduction of plasma aldosterone concentration which was related significantly to the increase of serum potassium level (r = -0.533), but only weakly to the reduction of plasma angiotensin II level (r = 0.474). Aldosterone level remained suppressed in the face of increased serum potassium. The effects on aldosterone level and potassium were greater in patients with high plasma renin activity than in those with low and normal plasma renin activities. They also paralleled the reduction in blood pressure. It is suggested that reduction in aldosterone level and potassium retention were caused by blockade of angiotensin II formation by captopril, but the potassium retention was additionally influenced by renal impairment.
对23例高血压患者在恒定的钠钾饮食条件下口服血管紧张素转换酶抑制剂卡托普利(或SQ 14225)。结果显示血浆醛固酮浓度降低,这与血清钾水平升高显著相关(r = -0.533),但与血浆血管紧张素II水平降低的相关性较弱(r = 0.474)。面对血清钾升高,醛固酮水平仍受到抑制。血浆肾素活性高的患者,其醛固酮水平和钾的变化比血浆肾素活性低及正常的患者更明显。这些变化也与血压降低平行。提示卡托普利通过阻断血管紧张素II的形成导致醛固酮水平降低和钾潴留,但钾潴留还额外受肾功能损害的影响。