부산대학교 도서관

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1067/mai.2002.121316 Byline: Allen P. Kaplan, Kusumam Joseph, Michael Silverberg Keywords: Bradykinin; factor XII; prekallikrein; kininogen; kininase; angioedema Abbreviations: ACE:, Angiotensin-converting enzyme; Factor XIIf:, Factor XII fragment (Hageman factor fragment); gC1qR:, Receptor for the globular heads of the C1q subcomponent of complement; HAE:, Hereditary angioedema; HK:, High-molecular-weight kininogen; HUVEC:, Human umbilical cord endothelial cell; LK:, Low-molecular-weight kininogen; u-PAR:, Urokinase plasminogen activator receptor Abstract: Bradykinin is formed by the interaction of factor XII, prekallikrein, and high-molecular-weight kininogen on negatively charged inorganic surfaces (silicates, urate, and pyrophosphate) or macromolecular organic surfaces (heparin, other mucopolysaccharides, and sulfatides) or on assembly along the surface of cells. Catalysis along the cell surface requires zinc-dependent binding of factor XII and high-molecular-weight kininogen to proteins, such as the receptor for the globular heads of the C1q subcomponent of complement, cytokeratin 1, and urokinase plasminogen activator receptor. These 3 proteins complex together within the cell membrane, and initiation depends on autoactivation of factor XII on binding to gC1qR (the receptor for the globular heads of the C1q subcomponent of complement). There is also a factor XII-independent bypass mechanism requiring a cell-derived cofactor or protease that activates prekallikrein. Bradykinin is degraded by carboxypeptidase N and angiotensin-converting enzyme. Angioedema that is bradykinin dependent results from hereditary or acquired C1 inhibitor deficiencies or use of angiotensin-converting enzyme inhibitors to treat hypertension, heart failure, diabetes, or scleroderma. The role for bradykinin in allergic rhinitis, asthma, and anaphylaxis is to contribute to tissue hyperresponsiveness, local inflammation, and hypotension. Activation of the plasma cascade occurs as a result of heparin release and endothelial-cell activation and as a secondary event caused by other pathways of inflammation. (J Allergy Clin Immunol 2002;109:195-209.) Author Affiliation: Charleston, SC, and Stony Brook, NY From the Konishi-MUSC Institute for Inflammation Research, Division of Pulmonary and Critical Care Medicine and Allergy and Clinical Immunology, Department of Medicine, Medical University of South Carolina, and the Department of Medicine, State University of New York at Stony Brook Article History: Received 4 October 2001; Revised 19 October 2001; Accepted 25 October 2001 Article Note: (footnote) [star] Reprint requests: Allen P. Kaplan, MD, Medical University of South Carolina, Department of Medicine, Division of Pulmonary/Allergy, 96 Jonathan Lucas St, PO Box 250623, Charleston, SC 29425., [star][star] (Supported by a grant from Merck & Co, Inc, West Point, Pa), a Series editor: Lanny J. Rosenwasser, MD