依那普利拉对缺血大鼠心脏再灌注后缓激肽和去-精氨酸9-缓激肽释放的影响。
Effect of enalaprilat on bradykinin and des-Arg9-bradykinin release following reperfusion of the ischaemic rat heart.
作者信息
Lamontagne D, Nadeau R, Adam A
机构信息
Faculté de pharmacie, Université de Montréal, Québec, Canada.
出版信息
Br J Pharmacol. 1995 Jun;115(3):476-8. doi: 10.1111/j.1476-5381.1995.tb16357.x.
Abstract
- The release of bradykinin (BK) and its metabolite, des-Arg9-bradykinin (des-Arg9-BK), was studied following reperfusion of a globally ischaemic rat heart. 2. BK-like immunoreactivity increased from 13 +/- 3 (preischaemic value) to 48 +/- 12 fmol min-1 g-1 (P < 0.05, n = 14) 30 s after reperfusion. No difference in BK release was found between control hearts and hearts pretreated with the angiotensin converting enzyme (ACE or kininase II) inhibitor, enalaprilat (50 ng ml-1). 3. No significant change in des-Arg9-BK-like immunoreactivity during reperfusion was observed in control hearts. In contrast, des-Arg9-BK-like immunoreactivity rose from 44 +/- 15 to 177 +/- 61 fmol min-1 g-1 (P < 0.05, n = 7) 30 s after reperfusion in enalaprilat-treated hearts. 4. In conclusion, BK is released upon reperfusion of the globally ischaemic rat heart. ACE inhibitors, through the inhibition of kininase II, increase the formation of the active metabolite, des-Arg9-BK.
摘要
- 研究了全脑缺血大鼠心脏再灌注后缓激肽（BK）及其代谢产物去-精氨酸9-缓激肽（des-Arg9-BK）的释放情况。2. 再灌注30秒后，BK样免疫反应性从13±3（缺血前值）增加到48±12 fmol min-1 g-1（P<0.05，n = 14）。在对照心脏和用血管紧张素转换酶（ACE或激肽酶II）抑制剂依那普利拉（50 ng ml-1）预处理的心脏之间，未发现BK释放有差异。3. 在对照心脏中，再灌注期间des-Arg9-BK样免疫反应性无显著变化。相比之下，在依那普利拉处理的心脏中，再灌注30秒后des-Arg9-BK样免疫反应性从44±15上升到177±61 fmol min-1 g-1（P<0.05，n = 7）。4. 总之，全脑缺血大鼠心脏再灌注时会释放BK。ACE抑制剂通过抑制激肽酶II，增加了活性代谢产物des-Arg9-BK的形成。
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