Abstract
Reduced risk of myocardial infarction (MI) mortality with angiotensin-converting enzyme (ACE) inhibition suggests a link between the renin-angiotensin-system (RAS) and fibrinolytic function. Excessive endothelial production of plasminogen activator inhibitor type 1 (PAI-1) and deficient endothelial secretion of tissue-type plasminogen activator (t-PA) are associated with thrombosis and ischemic events, such as stroke, atherosclerosis, and MI. Angiotensin II (A-II) regulates PAI-1 production. Suppression of A-II formation by ACE inhibitors likely has a positive effect on Fibrinolytic balance by reducing the production of PAI-1. ACE inhibition also enhances bradykinin levels, which, in turn, increases t-PA secretion and further reduces thrombotic tendency.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 44-49 |
| Number of pages | 6 |
| Journal | Journal of Myocardial Ischemia |
| Volume | 7 |
| Issue number | SUPPL. 1 |
| State | Published - Jan 1 1995 |
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ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
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Thrombotic effects of angiotensin. / Vaughan, D. E.
In: Journal of Myocardial Ischemia, Vol. 7, No. SUPPL. 1, 01.01.1995, p. 44-49.Research output: Contribution to journal › Short survey
TY - JOUR
T1 - Thrombotic effects of angiotensin
AU - Vaughan, D. E.
PY - 1995/1/1
Y1 - 1995/1/1
N2 - Reduced risk of myocardial infarction (MI) mortality with angiotensin-converting enzyme (ACE) inhibition suggests a link between the renin-angiotensin-system (RAS) and fibrinolytic function. Excessive endothelial production of plasminogen activator inhibitor type 1 (PAI-1) and deficient endothelial secretion of tissue-type plasminogen activator (t-PA) are associated with thrombosis and ischemic events, such as stroke, atherosclerosis, and MI. Angiotensin II (A-II) regulates PAI-1 production. Suppression of A-II formation by ACE inhibitors likely has a positive effect on Fibrinolytic balance by reducing the production of PAI-1. ACE inhibition also enhances bradykinin levels, which, in turn, increases t-PA secretion and further reduces thrombotic tendency.
AB - Reduced risk of myocardial infarction (MI) mortality with angiotensin-converting enzyme (ACE) inhibition suggests a link between the renin-angiotensin-system (RAS) and fibrinolytic function. Excessive endothelial production of plasminogen activator inhibitor type 1 (PAI-1) and deficient endothelial secretion of tissue-type plasminogen activator (t-PA) are associated with thrombosis and ischemic events, such as stroke, atherosclerosis, and MI. Angiotensin II (A-II) regulates PAI-1 production. Suppression of A-II formation by ACE inhibitors likely has a positive effect on Fibrinolytic balance by reducing the production of PAI-1. ACE inhibition also enhances bradykinin levels, which, in turn, increases t-PA secretion and further reduces thrombotic tendency.
UR - http://www.scopus.com/inward/record.url?scp=0028820432&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028820432&partnerID=8YFLogxK
M3 - Short survey
AN - SCOPUS:0028820432
VL - 7
SP - 44
EP - 49
JO - Journal of Myocardial Ischemia
JF - Journal of Myocardial Ischemia
SN - 1045-7984
IS - SUPPL. 1
ER -