Swies J, Grodzińska L, Sławiński M, Gryglewski R J
Department of Pharmacology, N. Copernicus Academy of Medicine, Cracow.
Acta Physiol Pol. 1990;41(1-3):87-95.
An intravenous injection of kallikrein produced hypotensive and thrombolytic effects in anesthetized cats, using the blood superfused tendon technique. The thrombolytic action of kallikrein was mediated by an unstable substance. The generation of this substance was abolished by either acetylsalicylic acid (ASA) or aprotonin and enhanced by captopril. The hypotensive action of kallikrein was only partially inhibited by ASA. It is proposed that both these pharmacological effects of kallikrein are mediated by bradykinin which in turn releases prostacyclin from the endothelium. However, in contrast to the thrombolytic effect of kallikrein which is totally mediated by prostacyclin the hypotensive action of kallikrein depends not only on prostacyclin but also on another endothelium-derived vasorelaxant, e.g. EDRF.
采用血液灌流肌腱技术，对麻醉猫静脉注射激肽释放酶可产生降压和溶栓作用。激肽释放酶的溶栓作用由一种不稳定物质介导。该物质的生成可被乙酰水杨酸（ASA）或抑肽酶消除，而被卡托普利增强。激肽释放酶的降压作用仅被ASA部分抑制。有人提出，激肽释放酶的这两种药理作用均由缓激肽介导，缓激肽继而从内皮释放前列环素。然而，与激肽释放酶的溶栓作用完全由前列环素介导不同，激肽释放酶的降压作用不仅取决于前列环素，还取决于另一种内皮源性血管舒张剂，如内皮舒张因子（EDRF）。
