Rat cardiomyocytes (RCm) are primary cells derived from normal rat heart tissue and are plated in inserts or plates immediately after primary isolation.

C-type natriuretic peptide (CNP) is found to have a proapoptotic effect on neonatal RCm while endothelin-1 protects RCm against CNP-induced apoptosis¹. Coculturing skeletal muscle cells isolated from transgenic mice with RCm showed that some part of the skeletal muscle cells can transdifferentiate into cardiomyocytes and that direct cell-to-cell contact and contraction of neighboring cardiomyocytes are important for the transdifferentiation². Cardiac myofibrils extracted from freshly isolated adult rat ventricular myocytes were used to assess the actomyosin adenosine triphosphatase activity and phosphorylation of troponin I (TnI) and myosin light chain 2 (MLC2)³. Growth hormone was found to prolong the survival of rats with post infarction heart failure. This effect was associated with the attenuation of cardiomyocytes apoptosis in the surviving myocardium and enhanced left ventricle relaxation and pathologic interstitial remodeling⁴. A review of the transverse tubule function in mammalian cardiac myocytes is available⁵.