Transforming growth factor beta (TGFbeta) plays a pivotal role in the production of extra cellular matrix (ECM) proteins, which is a characteristic feature of heart failure. This study investigates the effect of TGFbeta stimulation on autochthonally expressed collagen I, fibronectin, laminin, elastin, and laminin receptor in adult ventricular cardiomyocytes and its influence on contractile function. Freshly isolated cardiomyocytes from adult rats were used to examine the expression of ECM proteins and MAP-kinase phosphorylation by Western blotting. dL/L was measured to examine contractile function. TGFbeta stimulation (1 ng and 10 ng) increased the expression of all measured ECM proteins after 24 h. Similarly induction with TGFbeta (10 ng) for 24 h impaired contractile function at a frequency of 1.0 to 2.0 Hz. The phosphorylation degree of p38 MAP-kinase and JNK was heightened after TGFbeta induction, but not that of ERK. Inhibition of p38 MAP-kinase with SB202190 (10 mM) reduced TGFbeta-induced fibronectin and elastin expression. Inhibition of JNK with SP600125 (10 mM) resulted in the reduction of laminin receptor expression. Cardiomyocytes are able to influence their outer milieu by themselves. High TGFbeta concentrations exert direct effects on both ECM deposition and contractile function. If these both parameters are linked together and which additional signalling molecules are involved is of further interest.