粗制激肽释放酶对离体兔主动脉条中血管紧张素I的肌otropic作用的增强作用。 （注：“myotropic”可能有误，推测原文可能是“myotropic”应是“myotrophic”，若如此，更准确译文为：粗制激肽释放酶对离体兔主动脉条中血管紧张素I的促肌营养作用的增强作用 ）
Potentiation by crude kallikrein of the myotropic effect of angiotensin I in the isolated rabbit aortic strip.
作者信息
Ercan Z S, Türker R K
出版信息
Experientia. 1977 Mar 15;33(3):369-70. doi: 10.1007/BF02002832.
Crude kallikrein (Padutin), but not pure kallikrein, when preincubated with angiotensin I caused a potentiation of the myotropic effect of decapeptide on the isolated continuously superfused rabbit aortic strip. Addition of converting enzyme inhibitor, SQ 20881, to the medium inhibited this potentiation. The potentiation by crude kallikrein of the myotropic effect of angiotensin I is probably due to the conversion of decapeptide to octapeptide angiotensin II. This study indicates that Padutin is not a pure kallikrein preparation and probably contains a kininase fraction which causes the conversion of angiotensin I.
粗制激肽释放酶（缓激肽），而非纯激肽释放酶，在与血管紧张素I预孵育时，会增强十肽对离体持续灌注兔主动脉条的肌动效应。向培养基中添加转化酶抑制剂SQ 20881可抑制这种增强作用。粗制激肽释放酶对血管紧张素I肌动效应的增强作用可能是由于十肽转化为八肽血管紧张素II。本研究表明，缓激肽不是纯激肽释放酶制剂，可能含有一种能使血管紧张素I发生转化的激肽酶成分。
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