From several studies it is evident that AngII enhances TGFb1 expression, and that this pathway is involved in hypertrophic growth and cardiac fibrosis. We now continued characterization of the signaling pathway stimulated by AngII in ventricular cardiomyocytes of rat and analysed, if AngII may also contribute to apoptosis induction. Stimulation of myocytes with 100 nM AngII for 2 h activated the transcription factors AP-1 and GATA. Induction of both factors was blocked by the p38MAPK inhibitor SB202190. When GATA was inhibited by transformation of cardiomyocytes with decoy oligonucleotides AngII could not enhance TGFb1 mRNA and protein expression. In contrast to the early induction of GATA and AP-1, the transcription factor SMAD was induced by AngII after 24 h. This stimulation was dependent on TGFb1, because it was blocked by antibodies specific for TGFb1. Since SMADs have been shown to mediate apoptosis induction by TGFb1 we tested, if stimulation of this pathway by AngII also provokes apoptosis. Indeed, 24 h after AngII addition the number of apoptotic cardiomyocytes raised by 4.4 ± 1.3 %. In conclusion, signaling of AngII through TGFb1 stimulates apoptosis in ventricular cardiomyocytes. TGFb1 expression is regulated via p38 MAPK, and the transcription factors AP-1 and GATA.