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Am J Physiol Heart Circ Physiol 283: H156-H164, 2002. First published March 21, 2002; doi:10.1152/ajpheart.00848.2001
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Vol. 283, Issue 1, H156-H164, July 2002

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

Roger Gaertner, Fabrice Prunier, Monique Philippe, Liliane Louedec, Jean-Jacques Mercadier, and Jean-Baptiste Michel

Cardiovascular Research Department, Institut National de la Santé et de la Recherche Médicale, 75018 Paris, France

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 after 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 tissue 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.

experimental heart failure; cardiac remodeling


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