Unger T, Hübner D, Schüll B, Yukimura T, Rascher W, Lang R E, Ganten D
Am J Cardiol. 1982 Apr 21;49(6):1530-2. doi: 10.1016/0002-9149(82)90378-2.
Intravenous administration of captopril (20 micrograms) produced inhibition of angiontensin I pressor responses by 70 percent and of plasma-converting enzyme activity by 72 percent. Oral treatment with captopril (50 mg/kg/day) for 1 week inhibited angiotensin I pressor responses more (84 percent) than plasma-converting enzyme activity (23 percent). Four month oral treatment of normotensive and spontaneously hypertensive rats with captopril (50 mg/kg/day) led to 68 and 71 percent inhibition of angiotensin I pressor responses, but produced increases in plasma-converting enzyme activity of 123 and 94 percent, respectively. In spontaneously hypertensive rats, elevated converting enzyme activity in the medulla oblongata was measured after this treatment. It is concluded that plasma-converting enzyme activity measurements can be dissociated from the in vivo inhibition of converting enzyme. Chronic oral captopril treatment results in an induction of converting enzyme biosynthesis not only in peripheral tissue but also in the brain.
静脉注射卡托普利（20微克）可使血管紧张素I升压反应抑制70%，血浆转化酶活性抑制72%。以卡托普利（50毫克/千克/天）口服治疗1周，对血管紧张素I升压反应的抑制作用（84%）比对血浆转化酶活性的抑制作用（23%）更强。对正常血压和自发性高血压大鼠用卡托普利（50毫克/千克/天）进行4个月的口服治疗，可使血管紧张素I升压反应分别抑制68%和71%，但血浆转化酶活性分别升高123%和94%。在自发性高血压大鼠中，经此治疗后测量了延髓中升高的转化酶活性。得出的结论是，血浆转化酶活性的测量结果可能与转化酶在体内的抑制作用不相关。长期口服卡托普利治疗不仅会导致外周组织中转化酶生物合成的诱导，还会导致大脑中转化酶生物合成的诱导。
