© 2006 European Society of Cardiology
Functional alterations in NO, PGI2 and EDHF pathways in the aortic endothelium after myocardial infarction in rats
a Department of Experimental Pharmacology, Chair of Pharmacology, Jagiellonian University Medical College Grzegorzecka Str. 16, 31-531 Krakow, Poland
b Ludwig Boltzmann Cluster for Cardiovascular Research c/o Institute for Biomedical Research, Allgemeines Krankenhaus Wien, Waehringer Guertel 18-20, A-1090 Vienna, Austria
* Corresponding author. Tel.: +48 12 421 11 68; fax: +48 12 421 72 17. E-mail address: s.chlopicki{at}cyfronet.krakow.pl
 |
Abstract |
|---|
Background: Previous work on endothelial dysfunction in post-MI heart failure has shown conflicting results.
Aim: To analyze gender related alterations in NO-, PGI2- and EDHF-dependent endothelial function in the thoracic aorta 7 and 42 days after myocardial infarction (MI).
Methods and results: MI was induced by coronary artery ligation in female and male Sprague–Dawley rats. There was no gender related difference in infarct-size or in the impairment of fractional shortening of the left ventricle 42 days after coronary ligation. Neither acetylcholine-induced (Ach) vasodilation nor basal PGI2 production in the aorta was modified by coronary ligation. Interestingly, 7 days after MI, basal NO production was impaired and the EDHF component of Ach-induced vasodilation was up-regulated, in both male and female rats. However, 42 days post-MI, basal NO was only impaired in male rats, while EDHF was only up-regulated in female rats.
Conclusion: MI induced impairment of functional activity of basal NO production and adaptive up-regulation of the EDHF component of Ach-induced relaxation. The above alterations in endothelial function in the aorta were gender-specific at 42 days but not 7 days after MI. Some of the previously reported discrepancies in the development of endothelial dysfunction in the post-MI period may be gender related differences.
Key Words: Heart failure • Endothelial dysfunction • NO • PGI2 • EDHF • Gender
Received February 8, 2006; Revised July 3, 2006; Accepted September 19, 2006
1 The authors equally contributed to this work.
2 Current address: Department of Pathophysiology, Albert Szent-Gyorgyi Medical and Pharmaceutical Center, University of Szeged, Semmelweis u. 1., Pf., 427 H6701 Szeged, Hungary.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  D. López, A. Rodríguez-Sinovas, E. Agulló, Án. García, J. A. Sánchez, and D. García-Dorado Replacement of connexin 43 by connexin 32 in a knock-in mice model attenuates aortic endothelium-derived hyperpolarizing factor-mediated relaxation Exp Physiol, October 1, 2009; 94(10): 1088 - 1097. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. C Villar, A. J Hobbs, and A. Ahluwalia Sex differences in vascular function: implication of endothelium-derived hyperpolarizing factor J. Endocrinol., June 1, 2008; 197(3): 447 - 462. [Abstract] [Full Text] [PDF]
|
|