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Am J Physiol Heart Circ Physiol (March 21, 2002). doi:10.1152/ajpheart.00848.2001
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Articles in PresS, published online ahead of print March 21, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00848.2001
Submitted on September 28, 2001
Accepted on March 13, 2002

Scar and pulmonary expression and shedding of ACE in rat myocardial infarction

Roger Gaertner1, Fabrice Prunier1, Monique Philippe1, Liliane Louedec1, Jean-Jacques Mercadier1, and Jean-Baptiste Michel1*

1 Cardiovascular Remodelling, INSERM U460, Paris, France

* To whom correspondence should be addressed. E-mail: u460{at}bichat.inserm.fr.

We examined the topology of Angiotensin Converting Enzyme (ACE) mRNA expression, activity and shedding in myocardial infarction induced heart failure and sought to elucidate the source of the increased plasma ACE activity in this model. Three months following coronary ligature, lung, scar and remaining viable left ventricular tissues were analyzed for ACE mRNA expression as well as tissue and solubilized ACE activity. ACE mRNA expression increased in the scar with respect to infarct severity, decreased in the lung and remained unchanged in the left ventricle. ACE activity decreased in the lung and increased in the scar and plasma. Shedding of ACE remained constant in the lung and increased in the scar. This study shows that ACE expression and activity is shifted from the pulmonary endothelium to the infarct scar tissue and that constancy of shedding in the lung and its increase in the scar are the source of the increased plasma ACE in congestive heart failure.




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