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Human Molecular Genetics Advance Access originally published online on May 5, 2004
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Human Molecular Genetics, 2004, Vol. 13, No. 14 1441-1450
DOI: 10.1093/hmg/ddh147
Human Molecular Genetics, Vol. 13, No. 14 © Oxford University Press 2004; all rights reserved

Over-expression of angiotensin converting enzyme-1 augments cardiac hypertrophy in transgenic rats

Xiao-Li Tian1, Yigal Martin Pinto1, Olivier Costerousse1, Wolfgang M. Franz2, Andrea Lippoldt3, Sigrid Hoffmann3, Thomas Unger4 and Martin Paul1,*

1Department of Clinical Pharmacology, Benjamin Franklin Medical Center, Free University of Berlin, Berlin 12200, Germany, 2Department of Internal Medicine, University of Lübeck, Lübeck D-23538, Germany, 3Hypertension Research, Max-Delbrück Center (MDC) for Molecular Medicine, Berlin 13092, Germany and 4Department of Pharmacology, University of Kiel, Kiel 24105, Germany

Received March 5, 2004; Revised April 13, 2004; Accepted April 22, 2004

Increased cardiac angiotensin converting enzyme-1 (ACE1) is found in individuals who carry a deletion in intron 16 of ACE1 gene or in individuals who suffer from cardiac disorders, such as hypertrophy. However, whether a single increase in ACE1 expression leads to spontaneous cardiac defects remains unknown. To determine if the increased cardiac ACE1 actively plays a role or is merely the consequence of pathological changes in the process of cardiac hypertrophy, we generated a transgenic rat model with selective over-expression of human ACE1 in the cardiac ventricles. The left ventricular ACE1 activity is elevated about 50-fold in transgenic rats. Angiotensin-1 perfusion of isolated hearts demonstrated a significant decrease in coronary artery flow compared with non-transgenic littermates, suggesting that the transgenic ACE1 is functional. Neither cardiac hypertrophy nor other morphological abnormalities were observed in transgenic rats under standard living conditions. It was found, however, after induction of hypertension by suprarenal aortic banding, that the degree of cardiac hypertrophy in transgenic rats was significantly higher than that of banded control rats. The expressions of both ANF and collagen III, molecular markers of cardiac hypertrophy, were also increased in banded transgenic rats compared with banded control. Our results suggest that increased cardiac ACE1 does not trigger but augments cardiac hypertrophy.

* To whom correspondence should be addressed at: Charite Medical School, Campus Benjamin Franklin, Institute for Clinical Pharmacology, Garystrasse 5, 14167 Berlin, Germany. Tel: +49 30450570251; Fax: +49 30450570952; Email: tianx{at}ccf.org


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