血浆转换酶活性不能反映卡托普利口服治疗的效果。

Plasma-converting enzyme activity does not reflect effectiveness of oral treatment with captopril.

作者信息

Unger T, Schüll B, Hübner D, Yukimura T, Lang R E, Rascher W, Ganten D

出版信息

Eur J Pharmacol. 1981 Jun 19;72(2-3):255-9. doi: 10.1016/0014-2999(81)90282-x.

Abstract

Intravenous Captopril (20 microgram) in rats produced similar inhibition of the pressor responses to intravenous ANG I (70%) and of plasma-converting enzyme activity (CEA) measured fluorometrically (72%). One week oral treatment with Captopril (50 mg/kg per day) inhibited ANG I pressor responses more (84%) than plasma CEA (23%). Four-month oral treatment of normotensive and spontaneously hypertensive rats with Captopril (50 mg/kg per day) led to a 68% and 71% inhibition of the ANG I pressor responses, but to a 123% and 94% increase of plasma CEA, respectively. Thus, plasma CEA measurements can be dissociated from the in vivo inhibition of converting enzyme (CE). Chronic oral Captopril treatment induces CE biosynthesis.

摘要

大鼠静脉注射卡托普利（20微克）对静脉注射血管紧张素I的升压反应产生类似的抑制作用（70%），对用荧光法测定的血浆转化酶活性（CEA）也有类似抑制作用（72%）。卡托普利（每天50毫克/千克）口服治疗一周对血管紧张素I升压反应的抑制作用更强（84%），而对血浆CEA的抑制作用为23%。用卡托普利（每天50毫克/千克）对正常血压和自发性高血压大鼠进行四个月的口服治疗，分别导致血管紧张素I升压反应抑制68%和71%，但血浆CEA分别升高123%和94%。因此，血浆CEA测量结果可能与体内转化酶（CE）抑制作用不相关。长期口服卡托普利治疗可诱导CE生物合成。