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Abstract
Hageman factor (HF, factor XII), adsorbed to negatively charged agents, is transformed
to an activated state in which it initiates reactions of the intrinsic pathway of
thrombin formation by activating plasma thromboplastin antecedent (PTA, factor XI).
High-molecular-weight kininogen (HMWK, Fitzgerald factor) and plasma prekallikrein
accelerate these early steps in the clotting process. Questions have been raised about
the role of HMWK in the activation of Hageman factor by surfaces. In the present studies,
we report that the activation of purified human HF by sulfatides, ellagic acid, kaolin,
or glass occurred in the absence of HMWK. Indeed, small amounts of HMWK inhibited
activation of HF by ellagic acid. Physiological concentration of HMWK had little or
no influence on the activation of HF by sulfatides, kaolin, or glass, but higher concentrations
(3 to 6 times more) showed the same inhibitory effect as after activation by ellagic
acid. This inhibitory property of HMWK may be attributed to competitive binding of
HF and HMWK on the surface of the activating agents. In fact, when HF was added to
kaolin or glass that had been incubated with HMWK and then washed, the inhibitory
effect persisted, indicating HMWK that was bound to the surface blocked activation
of HF. Studies with 125I-HF and 125I-HMWK supported this interpretation. Plasma prekallikrein accelerated activation
of the amidolytic properties of HF by sulfatides, kaolin, or glass but did not influence
activation of HF by ellagic acid. In the presence of plasma kallikrein, HMWK at moderate
concentrations slightly accelerated the rate of activation of HF by activating agents
other than ellagic acid. Higher concentrations of HMWK counteracted both the accelerating effect of prekallikrein and the inhibitory effect observed when HF was incubated with an excess of kaolin. These experiments,
then, support the view that the procoagulant function of HMWK is localized to a point
subsequent to the activation of HF.
Abbreviations:
Hageman factor or factor XII ((HF)), plasma thromboplastin antecedent or factor XI ((PTA)), high-molecular-weight kininogen or Fitzgerald factor ((HMWK)), soybean trypsin inhibitor ((SBTI)), ovomucoid trypsin inhibitor ((OTI)), di-isopropylfluorophosphate ((DFP)), H-d-prolyl-l-phenylalanyl-l-arginine-p-nitroanilide ((HPPAN S-2302)), sodium dodecylsulfate-polyacrylamide gel electrophoresis ((SDS-PAGE)), barbital-saline buffer ((BS)), tris-(hydroxymethyl)-aminomethane ((Tris)), sodium ethylenediaminetetraacetic acid ((EDTA)), p-nitroaniline ((p-NA)), molecular weight ((MW)), diethylaminoethyl ((DEAE)), carboxymethyl ((CM))To read this article in full you will need to make a payment
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Article info
Publication history
Accepted:
May 31,
1983
Received:
September 30,
1982
Footnotes
☆This study was supported in part by research grant HL 01661 from the National Heart, Lung and Blood Institute, the National Institutes of Health, and in part by a grant from the American Heart Association.
Identification
Copyright
© 1983 Published by Elsevier Inc.
