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Cardiovascular Research Advance Access first published online on February 5, 2008
This version [Corrected Proof] published online on March 1, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn028
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Exercise training combined with angiotensin II receptor blockade limits post-infarct ventricular remodelling in rats

Xiaohua Xu1, Wenhan Wan1, Lisa Ji2, Shunhua Lao1, Anthony S. Powers1, Weiyan Zhao1, John M. Erikson3 and John Q. Zhang1,*

1 Laboratory of Cardiovascular Research, University of Texas at San Antonio, 1 UTSA Circle, San Antonio, TX 78249, USA
2 Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA
3 Division of Cardiology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA

* Corresponding author. Tel: +1 210 458 7390; fax: +1 210 458 5873. E-mail address: john.zhang{at}utsa.edu

Aims: Our aim was to test the hypothesis that angiotensin II receptor blockade combined with exercise training after myocardial infarction (MI) could attenuate post-MI left ventricular remodelling and preserve cardiac function.

Methods and results: Sprague–Dawley rats underwent ligation of the left descending coronary artery, resulting in MI, or a sham operation. Losartan treatment and exercise training were initiated 1 week after infarction and continued for 8 weeks, either as a single intervention or combined. Collagen volume fraction in the sedentary MI (MISed) group was significantly higher than other MI groups treated with exercise training and/or losartan. Compared with MISed group, hearts of rats receiving exercise and/or losartan treatment had lower tissue inhibitor of matrix metalloproteinase (TIMP) 1. Matrix metalloproteinase (MMP) 2 or MMP-9 did not differ among all groups. Additionally, the level of angiotensin II receptor type 1 (AT1) protein significantly decreased in response to exercise training. Furthermore, angiotensin converting enzyme (ACE) binding was markedly lower in hearts receiving exercise training than in the MISed hearts. Cardiac function was preserved in rats receiving exercise training, and the beneficial effect was further improved by exercise combined with losartan treatment in comparison to the MISed group.

Conclusion: Our results suggest that post-MI exercise training and/or AngII receptor blockade reduces TIMP-1 expression and mitigates the expressions of ACE and AT1 receptor. These improvements, in turn, attenuate myocardial fibrosis and preserve post-MI cardiac function.

KEYWORDS Myocardial infarction; Remodelling; Exercise; Angiotensin; Metalloproteinases

Time for primary review: 32 days


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