Muirhead E E, Brooks B, Brosius W L
Arch Pathol Lab Med. 1980 Dec;104(12):631-4.
Captopril (SQ 14225), a converting enzyme inhibitor, significantly lowered the arterial pressure (AP) of rats with angiotensin-salt hypertension, a hypertensive state associated with sodium retention, volume expansion, and suppression of both renin and aldosterone secretion. While captopril was acting, there was no increase in sodium, potassium, or water excretion. Thus, the antihypertensive effect was not due to natriuresis or diuresis. Moreover, as the AP was lowered, there was no change in plasma renin concentrtion, the pulse rate was lowered, and the lack of potassium retention suggested minimal or no effect on aldosterone secretion. The mechanism of action of captopril in a sodium-volume-expanded, renin-aldosterone-suppressed state is unknown.
卡托普利(SQ 14225),一种转换酶抑制剂,可显著降低患血管紧张素-盐性高血压大鼠的动脉血压(AP),血管紧张素-盐性高血压是一种与钠潴留、血容量扩张以及肾素和醛固酮分泌受抑制相关的高血压状态。在卡托普利发挥作用期间,钠、钾或水的排泄并未增加。因此,其降压作用并非由于利钠或利尿。此外,随着动脉血压降低,血浆肾素浓度并无变化,脉搏率降低,且不存在钾潴留,这表明对醛固酮分泌的影响极小或没有影响。卡托普利在钠-血容量扩张、肾素-醛固酮受抑制状态下的作用机制尚不清楚。