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INDUCES AN ALTERATION OF CARDIAC FUNCTIONS
1 Laboratoire de pharmacologie et physicochimie des interactions cellulaires et moleculaires, UMR-CNRS 7034, University Louis Pasteur Faculte de Pharmacie, Illkirch Graffenstaden, France
2 Institut de genetique et biologie moleculaire et cellulaire, CNRS, INSERM, University Louis Pasteur, Illkirch Graffenstaden, France; Institut Clinique de la souris, Illkrich Graffenstaden, France
* To whom correspondence should be addressed. E-mail: ramaroson.andriantsitohaina{at}univ-angers.fr.
The peroxisome proliferator-activated receptor PPAR
plays a major role in the control of cardiac energy metabolism. The role of PPAR on cardiac functions was evaluated using PPAR knockout mice (PPAR (-/-)).
Haemodynamic parameters by sphygmomanometric measurements show that deletion of PPAR did not affect systolic blood pressure and heart rate. Echocardiographic measurements demonstrated reduced systolic performance as shown by the decrease of left ventricular fractional shortening in PPAR -/- mice. Telemetric electrocardiography revealed neither atrio- nor intra-ventricular conduction defects in PPAR -/- mice. Also, heart rate, P duration and amplitude, and QT interval were not affected. However, the amplitude of T-wave from PPAR -/- mice was lower compared to wild type mice (PPAR +/+). When the myocardial function was measured by ex vivo Langendorff's heart preparation, basal and 
-adrenergic agonist-induced developed forces were significantly reduced in PPAR null mice. In addition, Western blot analysis shows that the protein expression of 1 adrenergic receptor is reduced in hearts from PPAR -/-. Histological analysis showed that hearts from PPAR -/- but not PPAR +/+ displayed myocardial fibrosis.
These results suggest that PPAR null mice have an alteration of cardiac contractile performance under basal and under stimulation of 1 adrenergic receptors. These effects are associated with myocardial fibrosis. The data shed light on the role of PPAR in maintaining cardiac functions.
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