| Target organ damage in hypertension: pathophysiology and implications for drug therapy. | |
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MedLine Citation:
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PMID: 16729871 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Hypertension is a well known risk factor for cardiovascular and cerebrovascular events such as heart attacks and strokes. In addition, it is associated with earlier changes in organ systems in the body, such as left ventricular hypertrophy (LVH), proteinuria and renal failure, retinopathy and vascular dementia which are grouped under the term "target organ damage" (TOD). There are many processes involved in the pathogenesis of TOD and these include endothelial activation, platelet activation, increased thrombogenesis, changes in the renin aldosterone angiotensin system (RAAS), and collagen turnover. All these changes work hand in hand and lead to the production of hypertensive TOD. In this review, we aim to provide an overview of the recent advances in pathophysiology of hypertensive TOD, and examine how these changes lead to the production of TOD. A better understanding of these pathogenic processes would help us better devise treatment strategies in preventing the dreaded complications associated with hypertension. |
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Authors:
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Sunil K Nadar; Muzahir H Tayebjee; Franz Messerli; Gregory Y H Lip |
Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Current pharmaceutical design Volume: 12 ISSN: 1381-6128 ISO Abbreviation: Curr. Pharm. Des. Publication Date: 2006 |
Date Detail:
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Created Date: 2006-05-29 Completed Date: 2006-06-15 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9602487 Medline TA: Curr Pharm Des Country: Netherlands |
Other Details:
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Languages: eng Pagination: 1581-92 Citation Subset: IM |
Affiliation:
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Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham B18 7QH, UK. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Blood Platelets
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physiology Dementia, Vascular / etiology* Endothelium, Vascular / physiology Humans Hypertension / complications*, drug therapy* Hypertrophy, Left Ventricular / etiology* Kidney Failure / etiology* Matrix Metalloproteinases / metabolism Neovascularization, Physiologic Proteinuria / etiology* Retinal Diseases / etiology* Thrombosis / etiology |
| Chemical | |
Reg. No./Substance:
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EC 3.4.24.-/Matrix Metalloproteinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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