Angiotensin, fibrinolysis, and vascular homeostasis.
There is strong evidence that imbalance of the fibrinolytic system is involved in the pathogenesis of ischemic cardiovascular events. A reduction in fibrinolytic function may also mediate part of the adverse response of the vasculature to conditions of low nitric oxide production. Because reduced nitric oxide activity predisposes to the development of atherosclerosis, imbalance of the fibrinolytic system is heavily implicated in the development of cardiovascular pathology. The renin-angiotensin system exerts substantial control over the fibrinolytic system, and pharmacologic interventions that reduce the activity of angiotensin II also have favorable effects on fibrinolytic balance and on the incidence of adverse cardiovascular events. This review summarizes the evidence for a link between activation of the renin-angiotensin system, fibrinolytic imbalance, and cardiovascular pathology.
Vaughan
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DE
Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232-6300, USA.
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000809:Angiotensins / Q000502:physiology; D001161:Arteriosclerosis / Q000188:drug therapy / Q000503:physiopathology*; D005342:Fibrinolysis / Q000187:drug effects / Q000502:physiology*; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology*; D010959:Tissue Plasminogen Activator / Q000378:metabolism
D000806:Angiotensin-Converting Enzyme Inhibitors; D000809:Angiotensins; D009569:Nitric Oxide; D010959:Tissue Plasminogen Activator