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内源性缓激肽在血管紧张素转换酶抑制剂卡托普利急性降压作用中的作用——通过缓激肽竞争性拮抗剂评估

Role of endogenous bradykinins in the acute depressor effect of angiotensin converting enzyme inhibitor captopril--assessed by a competitive antagonist of bradykinin.

作者信息

Seino M, Abe K, Nushiro N, Omata K, Yoshinaga K

机构信息

Second Department of Internal Medicine, Tohoku University, School of Medicine, Sendai, Japan.

出版信息

Clin Exp Hypertens A. 1989;11(1):35-43. doi: 10.3109/10641968909035289.

Abstract

To examine whether a hypotensive effect of converting enzyme inhibitor captopril was mediated partly by a potentiation of endogenous bradykinin, a newly synthesized competitive antagonist of bradykinin (B 4147) was used in anesthetized rats. The injection of B 4147 alone (50 and 100 micrograms) elicited significant increases in blood pressure. Although the administration of captopril (1 mg/kg, i.v.) caused a decrease in mean arterial pressure (MAP), the injection of the kinin antagonist (50 and 100 micrograms) after the captopril produced an increase in MAP by an average of 42 and 47% of the initial fall induced by captopril, respectively. The hypertensive effect of B 4147 was enhanced in magnitude and duration after the captopril. These results suggest that an accumulation of endogenous kinins by captopril contributes partly to the acute hypotensive effect of converting enzyme inhibitors in anesthetized rats.

摘要

为了研究转化酶抑制剂卡托普利的降压作用是否部分由内源性缓激肽的增强介导,一种新合成的缓激肽竞争性拮抗剂(B 4147)被用于麻醉大鼠。单独注射B 4147(50和100微克)可引起血压显著升高。虽然静脉注射卡托普利(1毫克/千克)导致平均动脉压(MAP)下降,但在卡托普利注射后注射缓激肽拮抗剂(50和100微克)分别使MAP升高,平均为卡托普利引起的初始下降的42%和47%。在卡托普利之后,B 4147的升压作用在幅度和持续时间上均增强。这些结果表明,卡托普利使内源性激肽积累,这在一定程度上促成了转化酶抑制剂对麻醉大鼠的急性降压作用。

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