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Am J Physiol Heart Circ Physiol 280: H984-H991, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 3, H984-H991, March 2001

ETA-receptor blockade prevents matrix metalloproteinase activation late postmyocardial infarction in the rat

Bruno K. Podesser*, Deborah A. Siwik*, Franz R. Eberli, Flora Sam, Soeun Ngoy, Julie Lambert, Khahn Ngo, Carl S. Apstein, and Wilson S. Colucci

Cardiovascular Section, Boston University Medical Center, and Myocardial Biology Unit and Cardiac Muscle Research Laboratory, Boston University School of Medicine, Boston, Massachusetts 02118

Endothelin (ET) A (ETA) receptors activate matrix metalloproteinases (MMP). Since endothelin-1 (ET) is increased in myocardium late postmyocardial infarction (MI), we hypothesized that stimulation of ETA receptors contributes to activation of myocardial MMPs late post-MI. Three days post-MI, rats were randomized to treatment with the ETA-selective receptor antagonist sitaxsentan (n = 12) or a control group (n = 12). Six weeks later, there were rightward shifts of the left ventricular (LV) end-diastolic and end-systolic pressure-volume relationships, as measured ex vivo by the isovolumic Langendorff technique. Both shifts were markedly attenuated by sitaxsentan. In LV myocardium remote from the infarct, the activities of MMP-1, MMP-2, and MMP-9 were increased in the post-MI group, and the increases were prevented by sitaxsentan treatment. Expression of tissue inhibitor of MMP-1 was decreased post-MI, and the decrease was prevented by sitaxsentan treatment. Chronic post-MI remodeling is associated with activation of MMPs in myocardium remote from the infarct. Inhibition of ETA receptors prevents MMP activation and LV dilation, suggesting that ET, acting via the ETA receptor, contributes to chronic post-MI remodeling by its effects on MMP activity.

endothelin; left ventricle; remodeling

* B. K. Podesser and D. A. Siwik contributed equally to the study.




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