Evidence For and Against the Kinins as Endogenous Mediators of Arthritis

  • Marion E. Webster
  • Harriet M. Maling
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 8)


That the kallikreins, the specific endogenous enzymes which liberate the kinins, are capable of increasing capillary permeability has been known for three decades (1,2). However, it was not until the kinins were isolated and synthesized in the early 1960s that they were found to be among the most potent agents in this regard (3–9). Preliminary electron microscopic observations suggested that the kinins may increase capillary permeability by causing a marked discontinuity in the endothelium of the capillaries (with intact subendothelial membrane) (10). Other investigators have provided evidence to suggest that these polypeptides increase venous pressure (11) or elevate capillary hydrostatic pressure (12) which leads to the production of edema. Since the pharmacological properties of the kinins (13) are such that they can reproduce some, although not all, of the clinical symptoms of arthritis, these polypeptides, like other chemical mediators, may contribute to the inflammatory synovial reaction seen in arthritides of varying etiology.


Synovial Fluid Ellagic Acid Soybean Trypsin Inhibitor Kinin Level Urate Crystal 
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Copyright information

© Plenum Press, New York 1970

Authors and Affiliations

  • Marion E. Webster
    • 1
  • Harriet M. Maling
    • 1
  1. 1.Experimental Therapeutics Branch and Laboratory of Chemical PharmacologyNational Heart InstituteBethesdaUSA

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