Ibrahim M. Salman
Metabolic syndrome, driven by obesity and diabetes, is a major contributor to cardiovascular disease. While large arteries vascular dysfunction is a well-documented phenomenon of metabolic syndrome, vascular disease of smaller diameter arteries, which are key contributors to peripheral vascular resistance and blood pressure control, remains uncertain. Using in-vitro organ-bath preparation, this study, therefore, investigated functional responses of the superior mesenteric and right iliac arteries in a high fat diet (HFD)/streptozotocin-induced diabetes mellitus rat model. Five-week-old male Wistar albino rats (n=24) were fed with either HFD (45 kcal% fat) or control diet (10 kcal% fat) for 10 weeks. On week 7, 40mg/kg streptozotocin and saline were injected intraperitoneally into the HFD and control groups, respectively. Diabetic HFD rats displayed a time-dependent increase (p<0.01) in water intake, urine output and fasting blood glucose. Both mesenteric and iliac vasoconstrictor responses (N/g) to norepinephrine (1×10-9–3×10-5M), but not to the depolarizing signals of high K+ (5–120 mM), were greater (p<0.01) in the HFD group relative to controls. Mesenteric, but not iliac, endothelium-dependent vasorelaxation to acetylcholine (1×10-10–1×10-5M) was blunted (p<0.05) in the HFD rats compared with controls. In contrast, mesenteric and iliac endothelium-independent vasorelaxation responses to sodium nitroprusside (1×10-11–1×10-6M) remained comparable between groups. In conclusion, vascular functional responses across smaller diameter arteries are differentially expressed in metabolic syndrome, demonstrating upregulated vasoconstriction to adrenergic stimuli and/or impaired endothelium-dependent relaxation. These vascular abnormalities align with those previously described in larger arteries and could therefore further promote the development of cardiovascular disease in metabolic syndrome
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