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The plasma kallikrein–kinin system: its evolution from contact activation
Author(s) -
SCHMAIER A. H.,
MCCRAE K. R.
Publication year - 2007
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/j.1538-7836.2007.02770.x
Subject(s) - prekallikrein , high molecular weight kininogen , factor xii , kallikrein , microbiology and biotechnology , kininogen , hemostasis , coagulation , chemistry , angiogenesis , kinin , contact system , biochemistry , biology , cancer research , medicine , bradykinin , enzyme , receptor , mechanical engineering , engineering
Summary. The plasma kallikrein–kinin system consists of the proteins factor XII (FXII), prekallikrein (PK), and high molecular weight kininogen. It was first recognized as a surface‐activated coagulation system that is activated when blood or plasma interacts with artificial surfaces. Although surface‐activated contact activation occurs in vivo in the case of tissue destruction or a developing thrombus, the physiologic basis for the activation and function of this system has not been delineated. New investigations indicate that there is a proteolytic pathway on cells for PK activation independent of FXII. This pathway for PK with subsequent FXII activation indicates physiologic activities. These activities include blood pressure regulation and modulation of thrombosis risk independently of hemostasis. Furthermore, they include regulation of endothelial cell proliferation, angiogenesis and apoptosis through a cellular‐based, outside‐in signaling system. The present characterizations of this system, which incorrectly had been thought to initiate coagulation, represent an evolution of understanding in this field.