Johnston C I, Millar J A, McGrath B P, Matthews P G
Lancet. 1979 Sep 8;2(8141):493-6. doi: 10.1016/s0140-6736(79)91552-6.
Captopril, an orally active angiotensin-converting enzyme (ACE) inhibitor, was effective in the long-term reduction of blood-pressure in 17 patients with essential hypertension. The addition of hydrochlorothiazide produced a further hypotensive effect, and the combined treatment produced satisfactory control of the blood-pressure for eight months. Captopril prevented and reversed the secondary hyperaldosteronism and hypokalaemia induced by simultaneous diuretic administration, thus eliminating the need for potassium supplements. The fall in plasma-angiotensin-II and urinary aldosterone and rise in angiotensin I and plasma-renin provide biochemical evidence that captopril inhibits ACE in vivo. No change in circulating venous bradykinin levels could be detected. The hypotensive action of captopril is not mediated by changes in blood-bradykinin but may involve inhibition of the renin-angiotensin and kallikrein-kinin systems locally within the kidneys or blood vessels.
卡托普利是一种口服有效的血管紧张素转换酶(ACE)抑制剂,对17例原发性高血压患者具有长期降压效果。加用氢氯噻嗪可产生进一步的降压作用,联合治疗使血压得到了8个月的满意控制。卡托普利预防并逆转了同时使用利尿剂引起的继发性醛固酮增多症和低钾血症,从而无需补充钾。血浆血管紧张素II和尿醛固酮水平下降,血管紧张素I和血浆肾素水平升高,这为卡托普利在体内抑制ACE提供了生化证据。未检测到循环静脉缓激肽水平的变化。卡托普利的降压作用不是由血液缓激肽的变化介导的,可能涉及局部抑制肾脏或血管内的肾素-血管紧张素系统和激肽释放酶-激肽系统。