Objective · To investigate the remodeling of superior mesenteric artery (SMA) in cirrhotic portal hypertension (PHT) rats. Methods · The rats were divided into normal group (n=8), PHT group with CCl4 inhalation for 8 weeks (n=8) and PHT group with CCl4 inhalation for 12 weeks (n=10). After the model was established, hemodynamic parameters of all the rats were measured. The liver tissues of the three groups were prepared for paraffin section, and then stained with hematoxylin and eosin staining (H-E staining), Masson staining and Sirius Red staining, respectively. After frozen sections of SMA tissues were prepared, H-E staining was performed to quantitatively analyze the lumen diameter, wall thickness and area of SMA. Caldesmon expression was detected by immunohistochemistry. The expression of elastin, cleaved caspase-3 protein (apoptotic signal) and Ki-67 protein (proliferation signal) were detected by immunofluorescence, and caldesmon and elastin of SMA in liquid nitrogen were detected by Western blotting. Results · Compared with the normal control group, portal pressure increased and mean arterial pressure decreased in PHT group with CCl4 inhalation for 8 and 12 weeks (all P<0.05), which meant the PHT model was successfully established. Compared with the normal group, the thickness and area of SMA vessel wall and the expression of caldesmon and elastin in SMA were decreased, and the apoptosis signal of SMA smooth muscle cells was increased in PHT group with CCl4 inhalation for 12 weeks (all P<0.05). Conclusion · The vascular remodeling of SMA in PHT with cirrhosis is thinning, and the expression of related contractile structural proteins such as caldesmon and elastin decrease sharply, while apoptosis signal of smooth muscle layer increases and related damage is serious.