Prothrombotic effects of angiotensin

Adv Intern Med. 2000;45:419-29.

Abstract

In vitro and in vivo data provide compelling evidence for an interaction between the RAS and thrombosis. Furthermore, angiotensin and AT1 receptor blockers may influence platelet function. ACE is strategically poised to regulate these interactions. ACE catalyzes the conversion of Ang I to Ang II, which in turn stimulates the production of PAI-1, sensitizes platelets, promotes the production of superoxide radicals that scavenge free NO, and induces the expression of tissue factor. Conversely, ACE catalyzes the breakdown of bradykinin, a potent stimulus to t-PA secretion. These data suggest that clinical, genetic, or environmental factors (such as salt intake and medications) that alter ACE activity and Ang II production would be expected to impact on clotting and fibrinolytic mechanisms.

Publication types

  • Review

MeSH terms

  • Angiotensin I / antagonists & inhibitors
  • Angiotensin I / metabolism
  • Angiotensin II / biosynthesis
  • Angiotensin Receptor Antagonists
  • Angiotensins / physiology*
  • Blood Coagulation
  • Blood Platelets / physiology
  • Bradykinin / metabolism
  • Fibrinolysis
  • Fibrinolytic Agents / metabolism
  • Free Radical Scavengers / metabolism
  • Humans
  • Nitric Oxide / metabolism
  • Peptidyl-Dipeptidase A / metabolism
  • Plasminogen Activator Inhibitor 1 / biosynthesis
  • Renin-Angiotensin System / physiology
  • Serine Proteinase Inhibitors / biosynthesis
  • Superoxides / metabolism
  • Thrombosis / physiopathology*
  • Tissue Plasminogen Activator / metabolism

Substances

  • Angiotensin Receptor Antagonists
  • Angiotensins
  • Fibrinolytic Agents
  • Free Radical Scavengers
  • Plasminogen Activator Inhibitor 1
  • Serine Proteinase Inhibitors
  • Superoxides
  • Angiotensin II
  • Nitric Oxide
  • Angiotensin I
  • Peptidyl-Dipeptidase A
  • Tissue Plasminogen Activator
  • Bradykinin