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Contact activation: a revision

A H Schmaier1

  • 1Department of Internal Medicine, University of Michigan, Ann Arbor 48109-0724, USA. aschmaie@medmail.med.umich.edu

Thrombosis and Haemostasis
|July 1, 1997
PubMed
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The contact system, including kininogens and high-molecular-weight kininogen (HK), plays a minimal role in initiating hemostasis but modulates vascular biology and inhibits thrombin-induced platelet activation, potentially impacting thrombosis risk.

Area of Science:

  • Biochemistry
  • Hematology
  • Vascular Biology

Background:

  • The contact system's role in hemostasis initiation is debated.
  • Deficiencies in contact proteins can prolong activated partial thromboplastin time (APTT) and may be associated with thrombosis.
  • Kininogens and high-molecular-weight kininogen (HK) are key components of the contact system.

Purpose of the Study:

  • To present a revised view of the contact system's function.
  • To elucidate the role of kininogens and HK in vascular biology and thrombosis.
  • To clarify the mechanism of contact system activation on endothelial cells.

Main Methods:

  • Review and synthesis of existing literature on the contact system.
  • Analysis of the biological activities of kininogens, bradykinin (BK), and HK.

Related Experiment Videos

  • Investigation of prekallikrein activation on endothelial cells.

    • Main Results:

    • The contact system has limited involvement in initiating hemostasis.
    • Kininogens inhibit alpha-thrombin-induced platelet activation.
    • BK modulates vascular biology, inducing vasodilation and releasing tissue plasminogen activator and prostacyclin.
    • HK serves as a receptor for prekallikrein, facilitating its activation on endothelial cells.
    • Endothelial cell-associated enzymes activate prekallikrein, leading to urokinase and plasminogen activation.

    Conclusions:

    • The contact system's primary functions lie in vascular biology modulation and thrombosis risk, not hemostasis initiation.
    • Contact protein assembly on cell membranes, rather than a "physiologic, negatively charged surface," constitutes the activation platform.
    • Understanding these mechanisms offers new insights into hemostasis, thrombosis, and vascular regulation.