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How a damaged blood vessel wall contibutes to thrombosis and hypertenasion
1Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine City Hospital, Birmingham, United Kingdom. a.blann@bham.ac.uk
In order to maintain an anticoagulant nature, the healthy endothelium secretes factors such as tissue plasminogen activator, ADPase, and expresses membrane thrombomodulin. However, when damaged, it releases increased amounts of pro-coagulants such as von Willebrand factor. Similarly, the healthy endothelium uses nitric oxide, prostacyclin and other molecules to help maintain normal blood pressure, and these molecules also inhibit platelet activity. But a dysfunctional endothelium fails to produce these vasodilators so that vasospasm and hypertension can result. Thus the (damaged/dysfunctional) endothelium can contribute to Virchow's triad by failing to maintain an anticoagulant surface and in failing to correctly regulate blood pressure, factors that are likely to promote thrombosis and hypertension.
In order to maintain an anticoagulant nature, the healthy endothelium secretes factors such as tissue plasminogen activator, ADPase, and expresses membrane thrombomodulin. However, when damaged, it releases increased amounts of pro-coagulants such as von Willebrand factor. Similarly, the healthy endothelium uses nitric oxide, prostacyclin and other molecules to help maintain normal blood pressure, and these molecules also inhibit platelet activity. But a dysfunctional endothelium fails to produce these vasodilators so that vasospasm and hypertension can result. Thus the (damaged/dysfunctional) endothelium can contribute to Virchow's triad by failing to maintain an anticoagulant surface and in failing to correctly regulate blood pressure, factors that are likely to promote thrombosis and hypertension.
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