Clenbuterol induces cardiac hypertrophy with normal functional, morphological and molecular features

doi:10.1016/S0008-6363(97)00190-9

Cardiovascular Research 1998 37(1):115-122; doi:10.1016/S0008-6363(97)00190-9
© 1998 by European Society of Cardiology

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Clenbuterol induces cardiac hypertrophy with normal functional, morphological and molecular features

Kit Wong^a, Kenneth R Boheler^a, Jill Bishop^b, Mario Petrou^a and Magdi H Yacoub^a^,*

^aDivision of Cardiothoracic Surgery, National Heart and Lung Institute, Imperial College of Science, Technology and Medicine, London, UK
^bCentre for Cardiopulmonary Biochemistry, University College London, Rayne Institute, London, UK

^* Corresponding author, at: Department of Cardiac Surgery, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK. Tel.: +44 171 3518533; Fax: +44 171 3763442.

Objective: Several pharmacological agents have been shown toproduce ‘physiological’ or ‘pathological’hypertrophy based on their functional characteristics. The aimof this study was to examine the features of cardiac hypertrophyinduced by the selective β₂-adrenergic agonist, clenbuterol.Methods: Cardiac hypertrophy was induced in 7-week-old Sprague-Dawleyrats by daily injections of clenbuterol for 3 weeks. Thyroxineand isoproterenol were also used to produce cardiac hypertrophyto serve as positive controls for physiological and pathologicalhypertrophy, respectively. Left ventricular function was determinedusing an isolated rat heart preparation. Ventricular sampleswere used for morphological examination while interstitial collagenwas measured using high-pressure liquid chromatography. Expressionof sarcoplasmic reticulum Ca²⁺-ATPase2a (SERCA2a) and phospholamban(PLB) were measured by dot blot analysis. Results: Clenbuteroltreatment induced 26% left ventricular hypertrophy. These heartsdemonstrated normal systolic isovolumic parameters and diastolic(active relaxation and passive stiffness) function. In addition,left ventricular concentration of collagen and morphology wasnormal as were the expression of SERCA2a and PLB mRNA. Conclusion:These results suggest that clenbuterol-induced hypertrophy is‘physiological’ in terms of its function, extracellularstructure and gene expression.

KEYWORDS β₂-adrenergic agonist; Hypertrophy; Rat, ventricle

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