Role of angiotensin II in coagulation and fibrinolysis

Nancy J. Brown; Douglas E. Vaughan

doi:10.1023/A:1009757416302

Role of angiotensin II in coagulation and fibrinolysis

Nancy J. Brown, Douglas E. Vaughan^*

^*Corresponding author for this work

Medicine, Cardiology Division

Research output: Contribution to journal › Review article › peer-review

13 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	193-198
Number of pages	6
Journal	Heart Failure Reviews
Volume	3
Issue number	3
DOIs	https://doi.org/10.1023/A:1009757416302
State	Published - 1999

Keywords

ACE inhibition
Ang II Receptor blockade
Fibrinolysis
PAI-1
Platelet function
t-PA

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

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10.1023/A:1009757416302

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title = "Role of angiotensin II in coagulation and fibrinolysis",

abstract = "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.",

keywords = "ACE inhibition, Ang II Receptor blockade, Fibrinolysis, PAI-1, Platelet function, t-PA",

author = "Brown, {Nancy J.} and Vaughan, {Douglas E.}",

note = "Funding Information: Supported by grants from the National Institutes of Health (NIH HL-14192, HL-56963, and HL-51387). DEV is the recipient of a Clinical Investigator Award from the Department of Veterans Affairs Research Administration.",

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AU - Brown, Nancy J.

AU - Vaughan, Douglas E.

N1 - Funding Information: Supported by grants from the National Institutes of Health (NIH HL-14192, HL-56963, and HL-51387). DEV is the recipient of a Clinical Investigator Award from the Department of Veterans Affairs Research Administration.

PY - 1999

Y1 - 1999

N2 - 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.

AB - 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.

KW - ACE inhibition

KW - Ang II Receptor blockade

KW - Fibrinolysis

KW - PAI-1

KW - Platelet function

KW - t-PA

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JO - Heart Failure Reviews

JF - Heart Failure Reviews

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Role of angiotensin II in coagulation and fibrinolysis

Abstract

Keywords

ASJC Scopus subject areas

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