Skip Navigation

European Heart Journal 1990 11(Supplement B):84-93; doi:10.1093/eurheartj/11.suppl_B.84
Copyright © 1990 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 van Wijngaarden, J.
Right arrow Articles by Wesseling, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by van Wijngaarden, J.
Right arrow Articles by Wesseling, H.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1990 The European Society of Cardiology

Basic pharmacology of ACE-inhibitors with respect to ischaemic heart disease: Prostaglandins and bradykinin

J. van Wijngaarden, R. A. Tio, W. H. van Gilst, P. A. de Graeff, C. D. J. de Langen and H. Wesseling

Department of Pharmacology and Clinical Pharmacology, University of Groningen The Netherlands

J. van Wijngaarden MD, Department of Pharmacology and Clinical Pharmacology, University of Groningen, Bloemsingel 1, 9713 BZ Groningen, The Netherlands

Experimental evidence suggests that ACE-inhibitors possess cardioprotective properties. Since ACE-inhibitors can prevent bradykinin breakdown and can stimulate prostaglandin production, it is thought that these cardioprotective effects are mediated by bradykinin and prostaglandins. This article summarizes the results indicating that bradykinin and prostaglandins, although not the only factors, do play an important role in cardioprotection by ACE-inhibitors. Special attention is paid to the presence of the sulphydryl moiety of certain ACE-inhibitors. Probably, these sulphydryl group-containing ACE-inhibitors have an additional protective effect through an interaction with bradykinin or through scavenging of free radicals.

However, these cardioprotective effects have not yet been shown in patients with ischaemic heart dkease, although some studies indicate that ACE-inhibitors are also able to cause antiischaemic effects in patients. Further studies are required to establish the clinical importance of cardioprotection by ACE-inhibitors in ischaemic heart disease.

Key Words: ACE-inhibitors • prostaglandins • bradykinin • sulphydryl group • cardioprotection • ischaemic heart disease


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


This article has been cited by other articles:


Home page
Circ. Res.Home page
T. Szerafin, N. Erdei, T. Fulop, E. T. Pasztor, I. Edes, A. Koller, and Z. Bagi
Increased Cyclooxygenase-2 Expression and Prostaglandin-Mediated Dilation in Coronary Arterioles of Patients With Diabetes Mellitus
Circ. Res., September 1, 2006; 99(5): e12 - 317.
[Abstract] [Full Text] [PDF]


Home page
Eur J Heart FailHome page
M. Hurlen, T. Hole, I. Seljeflot, and H. Arnesen
Aspirin does not influence the effect of angiotensin-converting enzyme inhibition on left ventricular ejection fraction 3 months after acute myocardial infarction
Eur J Heart Fail, March 1, 2001; 3(2): 203 - 207.
[Abstract] [Full Text] [PDF]



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.