Objective p66shc (66-kilodalton isoform of Shc gene products) gene, encoding a phosphotyrosine signal adapter protein, is confirmed to extend life span by 30%. Our aim was to determine the expression of Shc-related phosphotyrosine adaptor proteins in rat vascular aging in order to elucidate the value of vascular aging in the diagnosis and treatment of atherosclerosis. Methods A total of 60 Wistar rats were divided into 4 groups according to age, that is 4, 10, 16 and 24 months old rats respectively. Aorta plasma levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were detected, and the compliance of rat carotid segment was measured by constant liquid injection. Western blotting was used to detect the expression of p66shc and caspase-3 in the healthy rats of different ages. Results With aging, aorta wall was thickened with more severe fibrosis. MDA content in the rats of 16 and 24 months old was evidently ascended when compared with 4 and 10 months old (P＜0.01), but that of SOD was markedly declined (P＜0.01 compared with that of 4 month old rats; P＜0.05 compared with that of 10 month old rats). The carotid flexibility was increased, especially flexibility area was significantly different (P＜0.01 compared with that of 4 month old rats; P＜0.05 compared with that of 10 month old rats). The expression of p66shc and Caspase-3 at protein level was increased in a time-dependent manner. Conclusion The molecular mechanism of vascular aging might be associated with up-regulaton of p66shc and Caspase-3 with aging. Its underlying mechanism may provide theoretical basis for slowing down of vascular aging, and prevention and treatment of atherosclerosis.