Abstract
Kallikrein-kinin system has been suggested widely related to pathological conditions. Some of its related pathological significance were reviewed by Kallermeyer and Graham (1), and by Webster (2). Although the activation process of kallikreinogen in human plasma has not been well established, Webster and Ratnoff (3) suggested that Hageman factor (HF) was necessary to convert human kallikreinogen into activated kallikrein. It was also suggested that HF would activate plasminogen (4) and permeability factor/dilute (PF/dil) (5) in the early stage followed by the successive activation of kallikreinogen by these enzymes and, on the contrary, human plasma kallikrein converted human plasminogen to plasmin (6). On the other hand, Nagasawa et al. observed that HF directly activated bovine kallikreinogen to kallikrein (7). Some reasons for these confused observations may be partly due to the heterogeneity of plasma kininogenases (2, 8–11) and/or the substrate specificities of these enzymes (12, 13). The clear illustration on plasma kininogenases and of intrinsic kinin system in plasma were not obtained yet and remain to be discussed including the problems of species difference and activation methods.
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Moriya, H., Hojima, Y. (1972). Studies on Kinin-Forming Enzymes in Human Plasma and their Heterogeneity. In: Back, N., Sicuteri, F. (eds) Vasopeptides. Advances in Experimental Medicine and Biology, vol 21. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-7439-8_21
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DOI: https://doi.org/10.1007/978-1-4684-7439-8_21
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