Angiotensin II and the control of cardiovascular structure
The structure and function of the vessel wall are dependent on the balance of several counteracting forces, i.e., vasoconstricting versus vasodilating, growth-promoting versus growth-inhibiting, and proapoptotic versus antiapoptotic. In a normal healthy vessel, these factors are closely balanced. Ho...
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Published in | Journal of the American Society of Nephrology Vol. 10; pp. 120 - 128 |
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Main Author | |
Format | Conference Proceeding Journal Article |
Language | English |
Published |
Hagerstown, MD
Lippincott Williams & Wilkins
1999
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Subjects | |
Online Access | Get full text |
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Summary: | The structure and function of the vessel wall are dependent on the balance of several counteracting forces, i.e., vasoconstricting versus vasodilating, growth-promoting versus growth-inhibiting, and proapoptotic versus antiapoptotic. In a normal healthy vessel, these factors are closely balanced. However, under pathophysiologic conditions this balance is upset, resulting in the development of vascular hypertrophy and the generation of vascular lesions. For example, during the initiation and progression of atherosclerosis, there is an imbalance in a number of these processes, resulting in a proatherogenic state. Similarly, processes involved in maintaining the structure and function of the cardiac wall are under tight control and, when the control is upset, can result in left ventricular hypertrophy, with subsequent decreases in cardiac function and the development of failure. Evidence suggests that angiotensin II (AngII), acting via a family of receptors, plays an important role in the regulation of structure and function in both the heart and vessel wall; under pathologic conditions, the ability of the heart and vessel wall to generate AngII is increased, because of increased angiotensin-converting enzyme expression. In this review, the potential role of AngII in the regulation of cardiac and vascular structure and function is discussed. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 1046-6673 1533-3450 |