Skip Navigation

European Heart Journal 2003 24(4):294-296; doi:10.1016/S0195-668X(02)00630-9
Copyright © 2003 by the European Society of Cardiology.
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Related articles in EHJ
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
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 arrow Search for citing articles in:
ISI Web of Science (2)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Berger, R
Right arrow Articles by Pacher, R
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Berger, R
Right arrow Articles by Pacher, R
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Editorial

The role of the endothelin system in myocardial infarction—new therapeutic targets?

R Berger* and R Pacher

University Hospital of Vienna, Vienna, Austria

Received August 26, 2002; accepted August 28, 2002 * Corresponding author. Department of Cardiology, University of Vienna, Wahringer Gurtel 18-20, A-1090 Vienna, Austria. Tel.: +431-40400-4614; fax: +431-4081148
rberger@gmx.at

The first 10% of the full text of this article appears below.

See doi:10.1016/S1095-668X(02)00420-7for the article to which this editorial refers.

Endothelin (ET)-1, a 21-amino acid peptide, represents the major isoform of the endothelin peptide family, which further includes ET-2, ET-3, and ET-4.1 It is the most potent vasoconstrictor known and stimulates cell proliferation in various tissues. The biologically inactive precursor big ET is converted to the mature peptide by the endothelin-converting-enzyme. ETAreceptors, which lead to increased intracellular calcium concentrations, induce vasoconstriction and cell proliferation. ETBreceptors which mediate the release of NO and prostacyclin cause vasodilatation and are involved in the clearance of ET-1 and in the inhibition of the endothelin-converting-enzyme.

1. Endothelin and (coronary) atherosclerosis

In atherosclerosis, the production of ET-1 is stimulated and both tissue and plasma ET-1 levels are positively correlated with the extent of atherosclerosis.1 Moreover, in patients with coronaryartery . . . [Full Text of this Article]

2. Endothelin and myocardial infarction/remodelling


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

Related articles in EHJ:

Relationship between transcardiac gradient of endothelin-1 and left ventricular remodelling in patients with first anterior myocardial infarction
T. Tsutamoto, A. Wada, M. Hayashi, T. Tsutsui, K. Maeda, M. Ohnishi, M. Fujii, T. Matsumoto, T. Yamamoto, T. Takayama, C. Ishii, and M. Kinoshita
EHJ 2003 24: 346-355. [Abstract] [Full Text]  



This article has been cited by other articles:


Home page
 ChestHome page
I. A. Khan
Role of Endothelin-1 in Acute Myocardial Infarction
Chest, May 1, 2005; 127(5): 1474 - 1476.
[Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
A.-L. Hemdahl, E. Falk, P. Thoren, and G. K. Hansson
Thrombin inhibitor reduces myocardial infarction in apoE-/- x LDLR-/- mice
Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H872 - H877.
[Abstract] [Full Text] [PDF]