AJP - Heart Information on EB 2010
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 283: H156-H164, 2002. First published March 21, 2002; doi:10.1152/ajpheart.00848.2001
0363-6135/02 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
283/1/H156    most recent
00848.2001v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (13)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gaertner, R.
Right arrow Articles by Michel, J.-B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gaertner, R.
Right arrow Articles by Michel, J.-B.
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


This article has been cited by other articles:


Home page
 JNMHome page
Y. Chandrashekhar and J. Narula
Exposing ACE up the Sleeve...
J. Nucl. Med., February 1, 2007; 48(2): 173 - 174.
[Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
S. A. Dean, J. Tan, R. White, E. R. O'Brien, and F. H. H. Leenen
Regulation of components of the brain and cardiac renin-angiotensin systems by 17beta-estradiol after myocardial infarction in female rats
Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2006; 291(1): R155 - R162.
[Abstract] [Full Text] [PDF]

Home page
 Eur J Heart FailHome page
R. Gaertner, D. Lepailleur-Enouf, W. Gonzalez, A. Nicoletti, C. Mandet, M. Philippe, J.-J. Mercadier, and J.-B. Michel
Pulmonary endothelium as a site of synthesis and storage of interleukin-6 in experimental congestive heart failure
Eur J Heart Fail, August 1, 2003; 5(4): 435 - 442.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
K. Kohlstedt, F. Shoghi, W. Muller-Esterl, R. Busse, and I. Fleming
CK2 Phosphorylates the Angiotensin-Converting Enzyme and Regulates Its Retention in the Endothelial Cell Plasma Membrane
Circ. Res., October 18, 2002; 91(8): 749 - 756.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online