Calcification is an undesirable disorder, which frequently occurs in the heart vessels. In general, the formation of calcific vascular lesions involves complex physicochemical and molecular events. Calcification (hydroxyapatite) is initiated by injury and is progressed by promoter factors and/or the deficit of inhibitory signals. Myo-inositol hexakisphosphate (phytate, InsP₆) is found in organs, tissues and fluids of all mammals and exhibits an important capacity as a crystallization inhibitor of calcium salts in urine and soft tissues. The levels found clearly depend on the dietary intake but it can also be absorbed topically. In this paper, the capacity of InsP₆ as a potential inhibitor of cardiovascular calcifications was assessed in Wistar rats. Three groups were included, a control group, an InsP₆ treated group (subjected to calcinosis induction by Vitamin D and nicotine and treated with standard cream with a 2% of InsP₆ as potassium salt) and an InsP₆ non-treated group (only subjected to calcinosis induction). All rats were fed AIN 76-A diet (a purified diet in which InsP₆ is undetectable). Animals were monitorized every 12 hours. After 60 hours of calcinosis treatment, all rats of the InsP₆ non-treated group died and the rest were sacrificed. Aortas and hearts were removed. A highly significant increase in the calcium content of aorta and heart tissue was observed in the InsP₆ non-treated rats (21 +/- 1 mg calcium / g dry aorta tissue, 10 +/- 1 mg calcium / g dry heart tissue) when compared with controls (1.3 +/- 0.1 mg calcium / g dry aorta tissue, 0.023 +/- 0.004 mg calcium / g heart dry tissue) and InsP₆ treated (0.9 +/- 0.2 mg calcium / g dry aorta tissue, 0.30 +/- 0.03 mg calcium / g dry heart tissue) animals. Only InsP₆ non-treated rats displayed important mineral deposits in aorta and heart. These findings are consistent with the action of InsP₆, as an inhibitor of calcification of cardiovascular system.