Background and Objectives: Diabetes mellitus and hypertension are commonly associated and known as clustering of metabolic disorders. In this study, we aimed to determine the hemodynamic and pathologic effects of deoxycorticosterone acetate (DOCA)-salt and to determine the effect of chronic treatment of calcium channel blocker (CCB) and beta-blocker (BB) on hypertensive diabetic model. Methods: Otsuka Long-Evans Tokushima Fatty (OLETF) and age-matched Long-Evans Tokushima Otsuka (LETO) rats were treated with DOCA (25 mg/kg) with 1% NaCl in the drinking water after receiving a uninephrectomy. After 12-week treatment of DOCA-salt, blood pressure was measured. Then, CCB (clinidipine 30mg/kg/day) or BB (atenolol 25mg/kg/day) were given for additional 12 weeks without further administration of DOCA-salt. Total 24 weeks later, a media cross sectional area of aorta, myocardial fibrosis, and expressions of angiotensin II type 1 (AT1) and type 2 (AT2) receptor were evaluated. The expression of mRNA of 棺-myosin heavy chain, type IV collagen, AT1 receptor and AT2 receptor and reactive oxygen species were also determined. Results: DOCA-salt significantly increased systolic blood pressure (SBP) and diastolic blood pressure (DBP) in OLETF groups. However, in LETO groups, there were no significant changes of blood pressure parameters. Also, in OLETF with DOCA-salt groups, serum renin, angiotensin II levels were depressed and perivascular fibrosis was enhanced. However, these changes were not noted in LETO groups. The intima thickness of descending thoracic aorta was significantly increased in both LETO and OLETF groups after DOCA-salt administration. After stopping DOCA-salt for additional 12 weeks, blood pressure parameters were equalized between groups, including CCB and BB groups. But, In CCB and BB groups, the mRNA expression of AT2 receptor was decreased and intima thickness of descending thoracic aorta was significantly decreased. There was no significant differences in endothelial nitric oxide synthesis nor NAD(P)H subunits between groups. The AT1 and AT2 receptor expressions showed no significant differences between the drug administration groups. Conclusion: Underlying DM condition, hypertension may develop more easily in same condition. The perivascular fibrosis and intima thickness of descending thoracic aorta could be developed regardless of developing hypertension. The expression of angiotensin II type 2 receptor was depressed and aortic wall hypertrophy was regressed after CCB or BB treatment. Further study for the role of angiotensin II type 2 receptor would be needed in these models.