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Plasminogen Activator Inhibitor‐1: Physiologic Role, Regulation, and the Influence of Common Pharmacologic Agents
Author(s) -
Tsikouris James P.,
Suarez Jose A.,
Meyerrose Gary E.
Publication year - 2002
Publication title -
the journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.92
H-Index - 116
eISSN - 1552-4604
pISSN - 0091-2700
DOI - 10.1177/009127002762491271
Subject(s) - medicine , metformin , plasminogen activator inhibitor 1 , pravastatin , endocrinology , ace inhibitor , hyperinsulinemia , diabetes mellitus , plasminogen activator , estrogen , fibrinolysis , hypertriglyceridemia , angiotensin converting enzyme , tissue plasminogen activator , pharmacology , insulin resistance , blood pressure , cholesterol , triglyceride
Plasminogen activator inhibitor‐1 (PAI‐1) is the major inhibitor of endogenous thrombolysis, thereby promoting thrombosis. PAI‐1 is also a primary contributor to the development and recurrence of acute myocardial infarction. The renin angiotensin system, hypertriglyceridemia, hyperglycemia and hyperinsulinemia, and estrogen all influence the fibrinolytic system and PAI‐1 in particular. Available data strongly suggest that angiotensin‐converting enzyme (ACE) inhibitors and hormone replacement therapy with estrogen beneficially reduce PAI‐1 production. Metformin, an agent commonly used for non‐insulin‐dependent diabetes mellitus (NIDDM), appears to favorably decrease PAI‐1 production in NIDDM patients but not nondiabetic patients. Among the cholesterollowering statins, clinical literature evaluating pravastatin provides the most compelling data to support this agent's favorable effect on PAI‐1. Other available statins either have not displayed an effect on PAI‐1 or do not have clear data to conclusively define their effects on the fibrinolytic system.