| The prothrombotic paradox of hypertension: role of the renin-angiotensin and kallikrein-kinin systems. | |
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MedLine Citation:
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PMID: 16286563 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Despite increased pulsatile stress, thrombotic rather than hemorrhagic events represent a major complication of hypertension. The pathophysiology of thrombosis in hypertension involves the interaction among vascular endothelium and particularly the renin-angiotensin and kallikrein-kinin systems. Because hypertension is often associated with some degree of inflammation, the combination of chronic inflammation and chronic shear stress may convert the normal anticoagulant endothelium into a procoagulant surface, expressing tissue factor. Activation of the renin-angiotensin system leads to activation of nuclear factor kappaB-dependent proinflammatory genes, also accelerating the expression of tissue factor. Renin-angiotensin and kallikrein-kinin systems interact at several levels to modulate coagulation, fibrinolysis, and vasodilatation in such a way that these 2 systems could have a major influence on the occurrence of thrombotic complications. Treatment with angiotensin-converting enzyme inhibitors and angiotensin II type 1 receptor antagonists may favorably influence the balance between the renin-angiotensin and kallikrein-kinin axis, regulating blood pressure as well as reducing the risk of thrombosis, which may explain part of the clinical efficacy of these drugs. |
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Authors:
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Arne W J H Dielis; Machiel Smid; Henri M H Spronk; Karly Hamulyak; Abraham A Kroon; Hugo ten Cate; Peter W de Leeuw |
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Publication Detail:
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Type: Journal Article; Review Date: 2005-11-14 |
Journal Detail:
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Title: Hypertension Volume: 46 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2005 Dec |
Date Detail:
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Created Date: 2005-11-24 Completed Date: 2005-12-21 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 1236-42 Citation Subset: IM |
Affiliation:
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Department of Medicine, University Hospital Maastricht, Cardiovascular Research Institute Maastricht, University of Maastricht, The Netherlands. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Circulation Endothelium, Vascular / physiopathology Humans Hypertension / complications*, physiopathology Kallikrein-Kinin System Renin-Angiotensin System Thrombosis / etiology* |
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