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Kinin Formation: Mechanisms and Role in Inflammatory Disorders

Kinin Formation: Mechanisms and Role in Inflammatory Disorders Bradykinin and lysylbradykinin are potent vasoactive peptides liberated from !X2 globulins, called kininogens, by the actions of various proteases, known collectively as kininogenases. The pharmacologic properties of kinins-including their abilities to increase vascular permeability, to cause vasodilatation and pain, to contract most smooth muscle preparations, and to stimulate arachidonic acid metabolism-have led several inves­ tigators to suggest that these peptides may be important inflammatory mediators in humans (1 -3). Only in recent years, however, with improved assay technologies and an increased awareness of the mechanisms regu­ lating kinin levels, has meaningful direct evidence to support a role for the kinin system in human inflammatory disorders begun to accumulate. In the present chapter we review our current knowledge regarding the three different pathways that may lead to kinin formation in inflammatory events: (a) Generation of bradykinin as a result of the activation of the Hageman factor-dependent pathways and production of plasma kalli­ krein, (b) the generation of lysylbradykinin by tissue kallikreins, and (c) the potential role of cellular proteases in kinin formation. We also critically 49 0732--0582/88/0410-0049$02.00 PROUD & KAPLAN evaluate the evidence of activation of one or more pathways and the involvement of kinins during inflammatory disorders in http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Immunology Annual Reviews

Kinin Formation: Mechanisms and Role in Inflammatory Disorders

Proud, D; Kaplan, A P
Annual Review of Immunology , Volume 6 (1) – Apr 1, 1988
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Publisher
Annual Reviews
Copyright
Copyright 1988 Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0732-0582
eISSN
1545-3278
DOI
10.1146/annurev.iy.06.040188.000405
pmid
3289575
Publisher site
See Article on Publisher Site

Abstract

Bradykinin and lysylbradykinin are potent vasoactive peptides liberated from !X2 globulins, called kininogens, by the actions of various proteases, known collectively as kininogenases. The pharmacologic properties of kinins-including their abilities to increase vascular permeability, to cause vasodilatation and pain, to contract most smooth muscle preparations, and to stimulate arachidonic acid metabolism-have led several inves­ tigators to suggest that these peptides may be important inflammatory mediators in humans (1 -3). Only in recent years, however, with improved assay technologies and an increased awareness of the mechanisms regu­ lating kinin levels, has meaningful direct evidence to support a role for the kinin system in human inflammatory disorders begun to accumulate. In the present chapter we review our current knowledge regarding the three different pathways that may lead to kinin formation in inflammatory events: (a) Generation of bradykinin as a result of the activation of the Hageman factor-dependent pathways and production of plasma kalli­ krein, (b) the generation of lysylbradykinin by tissue kallikreins, and (c) the potential role of cellular proteases in kinin formation. We also critically 49 0732--0582/88/0410-0049$02.00 PROUD & KAPLAN evaluate the evidence of activation of one or more pathways and the involvement of kinins during inflammatory disorders in

Journal

Annual Review of Immunology – Annual Reviews

Published: Apr 1, 1988

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