Leslie B R, Case D B, Sullivan J F, Vaughan E D
Br Med J. 1980 Apr 19;280(6221):1067-8. doi: 10.1136/bmj.280.6221.1067.
Captopril, an orally active inhibitor of angiotensin-I-converting enzyme, was administered in a single dose to five anephric patients who had extremely low plasma renin activities. The drug did not lower blood pressure or significantly alter plasma renin activity in any patient but increased mean arterial pressure slightly in three. These results suggest that the blood-pressure lowering effect of captopril depends on an active renal renin-angiotensin system. Though additional mechanisms, such as accumulation of vasodilator kinins resulting from kininase II inhibition, may also contribute to captopril's action, these mechanisms apparently require the presence of the kidney to have a clinically detectable effect.
卡托普利是一种口服有效的血管紧张素I转换酶抑制剂,对五名血浆肾素活性极低的无肾患者给予单剂量该药。该药物未降低任何患者的血压或显著改变其血浆肾素活性,但有三名患者的平均动脉压略有升高。这些结果表明,卡托普利的降压作用取决于活跃的肾素-血管紧张素系统。虽然其他机制,如因激肽酶II抑制导致血管舒张性激肽的蓄积,可能也有助于卡托普利的作用,但这些机制显然需要肾脏的存在才能产生临床上可检测到的效果。