Nephrol Dial Transplant (2004) 19: 770-773
Nephrol Dial Transplant Vol. 19 No. 4 © ERA-EDTA 2004; all rights reserved
Editorial Comment
Reninangiotensin system and atherosclerosis
Abteilung Kardiologie und Angiologie, Medizinische Hochschule Hannover, Hannover, Germany
Correspondence and offprint requests to: Bernhard Schieffer, MD, Abteilung Kardiologie und Angiologie, Medizinische Hochschule Hannover, Carl-Neuberg-Strasse 1, D-30625 Hannover, Germany. Email: Schieffer.Bernhard@MH-Hannover.de
Keywords: angiotensin II; AT1 receptor; atherosclerosis; inflammation; reninangiotensin system
| The first 150 words of the full text of this article appear below. |
| Introduction |
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Cardiovascular (CV) events remain the main cause of morbidity and mortality in industrialized societies. Atherosclerosis is a chronic inflammatory disease [1] initiated and perpetuated by a variety of CV risk factors such as smoking, diabetes mellitus, hypertension and elevated plasma low-density lipoprotein (LDL) [2]. Atherosclerotic plaques are conglomerates composed of dysfunctional endothelial cells, smooth muscle cells, lipid-laden macrophages and T lymphocytes. These lipid-laden activated macrophages and T-lymphocytes stimulate their neighbouring cells to erode the collagen and elastin framework which forms the plaque's cap [15]. Myocardial infarction, stroke or sudden cardiac death are the fatal end-points of progressive atherosclerosis and are thought to be the result of these pathological remodelling processes [2]. Recent studies have identified morphological characteristics likely to be associated with a plaque's tendency to rupture, underlining the possibility of using such hallmarks clinically to predict, control and monitor
| Activation of the reninangiotensin system in atherosclerosis |
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| Why block the reninangiotensin system in atherosclerosis? |
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ACE inhibitors in atherosclerosis
AT1 antagonists in atherosclerosis
| Conclusion |
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