Abstract
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.
Keywords: platelet activation, endothelial activation, target organ damage, Hypertension
Current Pharmaceutical Design
Title: Target Organ Damage in Hypertension: Pathophysiology and Implications for Drug Therapy
Volume: 12 Issue: 13
Author(s): Sunil K. Nadar, Muzahir H. Tayebjee, Franz Messerli and Gregory Y.H. Lip
Affiliation:
Keywords: platelet activation, endothelial activation, target organ damage, Hypertension
Abstract: 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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Cite this article as:
Nadar K. Sunil, Tayebjee H. Muzahir, Messerli Franz and Lip Y.H. Gregory, Target Organ Damage in Hypertension: Pathophysiology and Implications for Drug Therapy, Current Pharmaceutical Design 2006; 12 (13) . https://dx.doi.org/10.2174/138161206776843368
DOI https://dx.doi.org/10.2174/138161206776843368 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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