Document Detail

The prothrombotic paradox of hypertension: role of the renin-angiotensin and kallikrein-kinin systems.
MedLine Citation:
PMID:  16286563     Owner:  NLM     Status:  MEDLINE    
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.
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:
Type:  Journal Article; Review     Date:  2005-11-14
Journal Detail:
Title:  Hypertension     Volume:  46     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2005 Dec 
Date Detail:
Created Date:  2005-11-24     Completed Date:  2005-12-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1236-42     Citation Subset:  IM    
Department of Medicine, University Hospital Maastricht, Cardiovascular Research Institute Maastricht, University of Maastricht, The Netherlands.
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MeSH Terms
Blood Circulation
Endothelium, Vascular / physiopathology
Hypertension / complications*,  physiopathology
Kallikrein-Kinin System
Renin-Angiotensin System
Thrombosis / etiology*

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