TY - JOUR
T1 - Prothrombotic effects of angiotensin
AU - Brown, Nancy J.
AU - Vaughan, Douglas E.
PY - 2000/12/1
Y1 - 2000/12/1
N2 - In vitro and in vivo data provide compelling evidence for an interaction between the RAS and thrombosis. Furthermore, angiotensin and AT 1 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-I, 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.
AB - In vitro and in vivo data provide compelling evidence for an interaction between the RAS and thrombosis. Furthermore, angiotensin and AT 1 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-I, 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.
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M3 - Article
C2 - 10635057
AN - SCOPUS:0033629311
VL - 45
SP - 419
EP - 429
JO - Advances in Internal Medicine
JF - Advances in Internal Medicine
SN - 0065-2822
ER -