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This Article Full Text Full Text (PDF) All Versions of this Article: 91/3/571    most recent expphysiol.2005.032607v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Stilli, D. Articles by Clément, S. Search for Related Content PubMed PubMed Citation Articles by Stilli, D. Articles by Clément, S. Related Collections Renal

¹ Dipartimento di Biologia Evolutiva e Funzionale-Sezione Fisiologia, Università di Parma, 43100 Parma, Italy² Department of Pathology, University of Geneva, 1211 Geneva, Switzerland

We have analysed alterations of -skeletal actin expression and volume fraction of fibrosis in the ventricular myocardium and their functional counterpart in terms of arrhythmogenesis and haemodynamic variables, in rats with different degrees of compensated cardiac hypertrophy induced by infra-renal abdominal aortic coarctation. The following coarctation calibres were used: 1.3 (AC_1.3 group), 0.7 (AC_0.7) and 0.4 mm (AC_0.4); age-matched rats were used as controls (C group). One month after surgery, spontaneous and sympathetic-induced ventricular arrhythmias were telemetrically recorded from conscious freely moving animals, and invasive haemodynamic measurements were performed in anaesthetized animals. After killing, subgroups of AC and C rats were used to evaluate in the left ventricle the expression and spatial distribution of -skeletal actin and the amount of perivascular and interstitial fibrosis. As compared with C, all AC groups exhibited higher values of systolic pressure, ventricular weight and ventricular wall thickness. AC_0.7 and AC_0.4 rats also showed a larger amount of fibrosis and upregulation of -skeletal actin expression associated with a higher vulnerability to ventricular arrhythmias (AC_0.7 and AC_0.4) and enhanced myocardial contractility (AC_0.4). Our results illustrate the progressive changes in the extracellular matrix features accompanying early ventricular remodelling in response to different degrees of pressure overload that may be involved in the development of cardiac electrical instability. We also demonstrate for the first time a linear correlation between an increase in -skeletal actin expression and the degree of compensated cardiac hypertrophy, possibly acting as an early compensatory mechanism to maintain normal mechanical performance.

(Received 13 October 2005; accepted after revision 30 January 2006; first published online 1 February 2006)
Corresponding author D. Stilli: Dipartimento di Biologia Evolutiva e Funzionale-Sezione Fisiologia, Università di Parma, Parco Area delle Scienze 11A, 43100, Parma, Italy. Email: donatella.stilli{at}unipr.it

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