Purdon A D, Schapira M, De Agostini A, Colman R W
J Lab Clin Med. 1985 Jun;105(6):694-9.
Recent evidence indicates that plasma kallikrein is activated during acute attacks of hereditary angioedema. Plasma kallikrein is known to convert inactive renin, or prorenin, into an active proteolytic enzyme in plasma exposed to acid or low temperatures as well as in purified systems. To establish whether plasma kallikrein could activate prorenin under physiologic or pathologic conditions, prorenin to renin conversion was assessed at neutral pH in plasma deficient in C1 inhibitor (hereditary angioedema). In these plasma samples lacking the two major inhibitors of kallikrein and possessing less than 10% of the inhibitory activity of normal plasma, prorenin was not converted to an active enzyme despite conditions under which prekallikrein was completely activated to plasma kallikrein and despite normal prorenin concentrations and activability.
最近的证据表明，在遗传性血管性水肿急性发作期间血浆激肽释放酶被激活。已知血浆激肽释放酶在暴露于酸或低温的血浆以及纯化系统中能将无活性的肾素（即血管紧张素原）转化为一种活性蛋白水解酶。为了确定血浆激肽释放酶在生理或病理条件下是否能激活血管紧张素原，在缺乏C1抑制剂（遗传性血管性水肿）的血浆中于中性pH下评估血管紧张素原向肾素的转化。在这些缺乏激肽释放酶的两种主要抑制剂且抑制活性不到正常血浆10%的血浆样本中，尽管前激肽释放酶完全被激活为血浆激肽释放酶，且血管紧张素原浓度和可激活性正常，但血管紧张素原并未转化为活性酶。
