Abstract
Clenbuterol, a β2-adrenoceptor (AR) agonist, has been employed in combination with other pharmacological agents and LVADs to treat patients with severe heart failure (HF). In experimental HF chronic clenbuterol (CLEN) administration induces cardiac hypertrophy and increases expression of Ca regulatory proteins resulting in improved contractility of isolated cardiac myocytes. However, the signaling pathway of CLEN remains undefined. The aims of this study were to assess the acute effects of CLEN on contractility in normal cardiomyocytes and use this to clarify its signaling pathways.
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