It was found in our study that the cardiac function at rest was not significantly affected in AT1-AA-treated rat offspring but recovery of the cardiac function from IRI was poorer and the area of myocardial infarction was larger, which are probably related to apoptosis- induced myocardial hypertrophy due to AT1-AA treatment during the fetal stage. The gene discussed is AGTR1; the disease is myocardial infarction.