Activation of the renin-angiotensin system increases the risk of atherohrombotic events in hypertensive patients. This relationship may be explained by multiple mechanisms, including effects on platelet function and on fibrinolysis. There is substantial evidence that angiotensin-converting enzyme (ACE) inhibitors may exert antithrombotic effects by enhancing the bradykinin-dependent release of tissue plasminogen activator (t-PA) while reducing the angiotensin-dependent production of its natural inhibitor PAI- 1, thus improving vascular fibrinolytic balance. Recent studies suggest that angiotensin (II) type 1 (AT1) receptor antagonists inhibit the effects of prothrombotic prostanoids. The antithrombotic effects of agents that block the RAS may contribute to their vasculoprotective properties.
- ACE inhibition
- Ang II Receptor blockade
- Platelet function
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine