Objective To study the mechanisms of vascular remodeling induced by hypertension and/or low shear stress, which will be helpful in the prevention, diagnosis and treatment of cardiovascular diseases. Method The models of low shear stress in carotid artery or of hypertension were established by the ligation of partial distal branches of the left common carotid artery (LCA) or by the coarctation of aorta in SD rats, respectively. For some rats, the low shear stress in LCA was accompanied by the hypertension. The wall thickness and the ratio of wall thickness to inner diameter were determined by morphometrical approach. The MMP-2 activity was detected by gel zymography, and the expression of proteins, including p-Akt, Rho GDIα, was verified by Western blotting in LCA. Results When LCA was subjected to hypertension or low shear stress, MMP-2 activity, the wall thickness, and the ratio of wall thickness to inner diameter were all increased significantly. They were further enhanced when the hypertension and low shear stress were both existed, which would speed the vascular remodeling. Low shear stress induced the expression of p Akt, and the lower shear stress, the higher p-Akt expression would be. However, the highest expression of p-Akt was observed in LCA of hypertension accompanied by low shear stress. The expression of Rho GDIα was upregulated in LCA by either low shear stress or hypertension. The highest expression of Rho GDIα was observed in LCA of hypertension accompanied by low shear stress. Conclusions Vascular remodeling could be mostly influenced in LCA subjected to low shear stress accompanied by hypertension, which was also regulated through the changing expression of p-Akt and Rho GDIα.