Skip Navigation

European Heart Journal 1995 16(Supplement K):23-30; doi:10.1093/eurheartj/16.suppl_K.23
Copyright © 1995 by the European Society of Cardiology.
This Article
Right arrow Full Text (PDF)
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Raynolds, M. V.
Right arrow Articles by Perryman, M. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Raynolds, M. V.
Right arrow Articles by Perryman, M. B.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1995 The European Society of Cardiology

The role of genetic variants in angiotensin I converting enzyme, angiotensinogen and the angiotensin II type-1 receptor in the pathophysiology of heart muscle disease

M. V. Raynolds and M. B. Perryman

University of Colorado Health Sciences Center Denver, Colorado, U.S.A.

Correspondence: Mary V. Raynolds, PhD, Assistant Professor, Division of Cardiology/Department of Medicine, University of Colorado Health Sciences Center, 4200 E. 9th Avenue, Denver, CO 80262, U.S.A.

The cardiac vasculature and myocardium contain components of the renin-angiotensin system (RAS), which may regulate local growth and cellular function. Alterations in the expression or action of these components which include angiotensin converting enzyme (ACE), angiotensinogen, and angiotensin II type-1 receptors may contribute to the development of disease; such as hypertension, left ventricular hypertrophy, myocardial infarction, and end-stage heart failure. ACE is one RAS component found to have genetic variants associated with cardiovascular disease. Molecular variants in any of the RAS components may affect signalling pathways possibly increasing the risk of heart failure. In addition, variants may exacerbate the deleterious effects of altered RAS expression on cardiac function. Genetic variation in RAS components may affect therapy with ACE inhibitors and receptor-blocking agents. Although at present there is no compelling reason to target molecular variations for treatment, a new era in selective pharmacological therapy for cardiovascular disease may be imminent.

Key Words: Angiotensin converting enzyme inhibitors • cardiovascular disease • genetic variants • heart failure • myocardial function • renin-angiotensin system


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.