Cardiac malformations (pulmonary trunk stenosis, ventricular septal defect, and double outlet right ventricle) were induced by the administration of two doses of retinoic acid (RA) to Wistar rats on d 13 of pregnancy. Contractile performance of the isolated perfused rat heart and its inotropic response to Ca2+ (0.6-10.0 mmol.L-1) was studied in 20-d-old fetuses. The body weight of RA-exposed fetuses was significantly lower compared with controls. RA negatively influenced the contractile parameters of the fetal rat heart. The most pronounced effect was, except at a Ca2+ concentration of 2.5 mmol.L-1, observed at developed force at all other concentrations. Simultaneously, the sensitivity to Ca2+, expressed as the Ca2+ concentration at which 30% of maximum was attained, ws significantly lower in RA-exposed hearts. This implies that the malformed heart is more dependent on the extracellular sources of Ca2+.