Aim To explore the effects of aging and hypertension on phenotypic switching of thoracic aortic vascular smooth muscle cell (VSMC) and regulation of VSMC phenotype by phosphatidylinositol 3-kinase (PI3K/Akt) and mitogen-activated protein kinase (MAPK) signaling pathway. Methods Male Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were studied at 1,3, 9,6 months of age, and each group had 12 rats. Blood pressure was noninvasively measured in the caudal artery. The thoracic aorta of rats in each group was taken for the experiment. HE staining was used to measure the wall thickness of the thoracic aorta. The expression and distribution of VSMC phenotype marker proteins α-smooth muscle-actin (α-SM-actin), calponin and osteopontin (OPN) were detected by immunohistochemical staining. Western blot was used to detect the expression of VSMC phenotype marker protein α-SM-actin, calponin, OPN, and signal proteins p-Akt, endothelial nitric oxide synthase (eNOS), p-42/44ERK and p-p38MAPK. Results HE staining showed that aging resulted in an increase in the thickness of vascular wall, and at 9 months old, there was a significant difference between WKY and SHR (P＜0.01). Immunohistochemical staining and Western blot showed that after 3 months old, the expressions of α-SM-actin and calponin in WKY and SHR decreased with the increase of age, while OPN increased; The expressions of p-Akt and eNOS proteins gradually decreased with the increase of age, and the expressions of p-42/44ERK and p-p38MAPK proteins increased gradually with the increase of age; At 3 months old, there was significant difference between the two groups (P＜0.01). Conclusion Aging and hypertension all contribute to the decreases in expressions of VSMC contractile phenotype marker proteins α-SM-actin and calponin, and the increase in the expression of VSMC synthetic phenotypic marker protein OPN in rat thoracic aorta. The interaction between aging and hypertension is more significant. The phenotypic switching of VSMC may be mediated by the balance between PI3K/Akt and MAPK signaling pathways.