Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow References
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 Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Ferrari, R.
Right arrow Articles by Ceconi, C.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Ferrari, R.
Right arrow Articles by Ceconi, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


Angiotensin II overproduction: enemy of the vessel wall

R. Ferraria,1, G. Guardigli1, G. Cicchitelli1, M. Valgimigli1, E. Merli1, O. Soukhomorskaia1 and C. Ceconi2

1 Chair of Cardiology, University of Ferrara, Ferrara, Italy
2 Cardiovascular Research Centre, Salvatore Maugeri Foundation, Gussago, Brescia, Italy

a Correspondence: Prof. Roberto Ferrari, Universita' di Ferrara, Arcispedale S. Anna, Corso Giovecca, 203, 44100 Ferrara, Italy.

Abstract

Unfortunately, the vessel wall has several enemies and, regrettably, overproduction of angiotensin II seems to be one of the most aggressive, often causing several principal diseases such as arteriosclerosis, hypertension, coronary artery disease and heart failure. Obviously, it is unrealistic to consider angiotensin II as the only player but, certainly, it is one of the most important, as the reduction of its overproduction by drugs such as ACE inhibitors or angiotensin II receptor blockers is able to counteract the above mentioned pathological conditions. This review mainly deals with the importance of overproduction of angiotensin II in causing endothelial dysfunction and the mechanisms which are involved, such as the activation of angiotensin I and II which have opposite effects. It is clear that a precise picture of the molecular changes induced by angiotensin II at tissue level cannot yet be described although progress is continuously made at the additive role of oxidative stress and activation of the nuclear factor {kappa}B is addressed. The mechanism of action of ACE inhibitors and the angiotensin II receptor blockers is also highlighted in the attitude which is considering the biological effect of these drugs and rather than their pharmacological effects.

Key Words: Angiotensin II • angiotensin-converting enzyme inhibitors


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.