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American Journal of Pathology, Vol 115, 92-101, Copyright © 1984 by American Society for Investigative Pathology

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Guinea pig plasma kallikrein as a vascular permeability enhancement factor. Its dependence on kinin generation and regulation mechanisms in vivo

T Imamura, T Yamamoto and T Kambara

Plasma kallikrein (mol wt 80,000) was purified from guinea pig plasma, and it caused vascular permeability enhancement when injected into guinea pig skin. The activity had a linear relationship to the logarithm of kallikrein concentrations from 5 X 10(-9) M to 5 X 10(-6) M and was blocked by immunopurified anti-prekallikrein F(ab')2 rabbit antibody and soybean trypsin inhibitor. Carboxypeptidase B(1.7 units), a kinin-destructive enzyme, decreased the permeability activity to 1/20, while SQ 20,881 (10(-6) M), an inhibitor to a kinin-destructive enzyme, augmented the activity 5.4-fold. These results suggested that the permeability activity of kallikrein was performed finally through kinin generation in the skin. The permeability activity was short- lasting, and was completely blocked by a kallikrein inhibitor purified from guinea pig plasma, suggesting the presence of a down-regulation system for the permeability activity in vivo. Prostaglandin E2 (25 ng), a hyperemia inducer in microcirculation, augmented the permeability activity 12-fold, suggesting the presence of an up-regulation system in vivo. Accordingly, it was assumed that kallikrein-kinin system might play a role as a vascular permeability enhancement system in guinea pig skin.


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Copyright © 1984 by the American Society for Investigative Pathology.