Aim To investigate the role of vascular smooth muscle cell phenotype transformation in carotid artery remodeling of Wistar rats fed by high salt diet, and the intervention of telmisartan. Methods The male Wistar rats were randomly divided into control group (0.5%NaCl feed), model group (4%NaCl feed), telmisartan group (4%NaCl and telmisartan 5 mg/(kg·day) feed). After 24 weeks, changes of morphology and structure of carotid artery were investigated by HE staining and Masson staining. The mRNA and protein levels of α-smooth muscle actin (α-SMA), smooth muscle 22α (SM22α) and osteopontin (OPN) were analyzed by quantitative real-time PCR and immunohistochemical staining. Results Compared with the control group, the blood pressure, media thickness, cross-sectional area, collagen volume fraction, and proliferating cell nuclear antigen (PCNA) positive cells were elevated in the model group. At the same time, the model group showed an increase in the mRNA and protein levels of α-SMA, SM22α, and a decrease of OPN. The telmisartan reduced the blood pressure, media thickness, cross-sectional area, collagen volume fraction, and the expression of PCNA and OPN, compared with the model group. Moreover, the mRNA and protein levels of α-SMA, SM22α were upregulated by telmisartan. Conclusions The 4% high salt diet can cause carotid artery remodeling and elevated-blood pressure in Wistar rats. The vascular smooth muscle phenotype transformation might be involved in the mechanism of carotid artery remodeling induced by high salt. Telmisartan can prevent artery remodeling partially via regulating vascular smooth muscle cell phenotypic transformation.