Obesity and diabetes constitute a hallmark of metabolic syndrome that is directly linked to vascular dysfunction and high blood pressure (BP). Accordingly, we aimed to investigate regional functional changes in thoracic and abdominal aortic responses in a rat model of high fat diet (HFD) and streptozotocin (STZ)-induced diabetes mellitus. Five weeks old male Wistar Albino rats (n = 24) were fed with either HFD (45 kcal% fat) or control diet (10 kcal% fat) for 10 weeks. At 10 weeks of age, 40 mg/kg STZ and saline were injected intraperitoneally into the HFD and control groups, respectively. At the end of the treatment, rats were euthanized to assess vasoconstrictor and vasodilator responses of dissected aortic segments.Conscious tail-cuff systolic BP was higher in the HFD relative to control (154 ± 6 mmHg vs. 110 ± 4 mmHg, p < 0.001). Oral glucose tolerance test (oGTT) generated greater AUCs in the HFD rats relative to controls (64,361 ± 383 vs. 14,169 ± 398, p < 0.001). Abdominal aortic vasoconstriction (N/g) to norepinephrine (NE, 1E-9 – 3E-5 M) and the depolarizing signals of high potassium (KCl, 5 – 120 mM) was greater (p < 0.05) in the HFD group compared with controls. Thoracic aortic vasoconstrictor responses (N/g) to NE, but not KCl, were greater (p < 0.05) in the HFD group as compared to controls. Abdominal, but not thoracic, endothelium-dependent vasorelaxation to acetylcholine (1E-10 – 1E-5 M) was blunted (p < 0.05) in the HFD group relative to controls. In contrast, thoracic and abdominal aortic responses to sodium nitroprusside (SNP)-induced endothelium-independent relaxation remained comparable between groups. Vascular functional responses are altered along the descending aorta in metabolic syndrome, exhibiting exaggerated vasocontractility and impaired endothelium-dependent relaxation. These vascular functional abnormalities could potentially underlie the development of hypertensive cardiovascular disease associated with the metabolic syndrome.