Bossaller C, Auch-Schwelk W, Gräfe M, Graf K, Baumgarten C, Fleck E
Department of Cardiology, German Heart Institute Berlin, Germany.
Agents Actions Suppl. 1992;38 ( Pt 3):171-7.
The effects of ACE-inhibitors on bradykinin metabolism and bradykinin-induced endothelium-dependent relaxation were studied in isolated coronary arteries and endothelial cells in culture. The results suggest that ACE-inhibitors affect coronary vascular tone by at least two endothelium-dependent and bradykinin-mediated mechanisms: First, ACE-inhibitors decrease endothelial bradykinin degredation which is accompanied by an augmented bradykinin mediated endothelium-dependent relaxation. Second, ACE-inhibitors evoke endothelium-dependent relaxations in coronary arteries stimulated with threshold concentrations of bradykinin, which cannot be attributed to an inhibition of bradykinin degradation. The effect appears to represent a new mechanism which may be based on an interaction of the bradykinin receptor and the angiotensin converting enzyme on the cellular level.
在离体冠状动脉和培养的内皮细胞中研究了血管紧张素转换酶抑制剂（ACE抑制剂）对缓激肽代谢及缓激肽诱导的内皮依赖性舒张的影响。结果表明，ACE抑制剂至少通过两种内皮依赖性和缓激肽介导的机制影响冠状动脉血管张力：第一，ACE抑制剂减少内皮缓激肽降解，同时缓激肽介导的内皮依赖性舒张增强。第二，ACE抑制剂在给予阈浓度缓激肽刺激的冠状动脉中引起内皮依赖性舒张，这不能归因于对缓激肽降解的抑制。该效应似乎代表一种新机制，可能基于缓激肽受体与血管紧张素转换酶在细胞水平上的相互作用。
