Adverse vascular remodelling is more sensitive than endothelial dysfunction to hyperglycaemia in diabetic rat mesenteric arteries

摘要: Increased vascular stiffness and reduced endothelial nitric oxide (NO) bioavailability are characteristic of diabetes. Whether these evident at a more moderate levels hyperglycaemia has not been investigated. The objectives this study were to examine the association between level glycaemia resistance vasculature phenotype, incorporating both arterial function. Diabetes was induced in male Sprague Dawley rats with streptozotocin (STZ; 55mg/kg i.v.) followed for 8 weeks. One week post STZ, diabetic allocated either (∼20mM blood glucose, 6-7U/insulins.c. daily) or severe (∼30mM 1-2U/insulins.c. daily as required). At end, anesthetized, mesenteric arcade collected. Passive mechanical wall properties assessed by pressure myography. Responses endothelium-dependent vasodilator acetylcholine (ACh) using wire Our results demonstrated first time that arteries from severely hyperglycaemic exhibited outward hypertrophic remodelling increased axial compared non-diabetic rats. Secondly, glucose), but moderately glucose) exhibit significant reduction ACh sensitivity their counterparts. This dysfunction associated endothelium-derived hyperpolarisation NO-mediated relaxation. Interestingly, nitroxyl (HNO)-mediated relaxation intact. Therefore, is sufficient induce adverse structural changes vasculature, essential cause dysfunction.