Abstract-Nitric oxide plays a pivotal role in regulating vascular tone. Different studies show endothelial function is impaired during hyperglycemia. Dark chocolate increases flow-mediated dilation in healthy and hypertensive subjects with and without glucose intolerance; however, the effect of pretreatment with dark chocolate on endothelial function and other vascular responses to hyperglycemia has not been examined. Therefore, we aimed to investigate the effects of flavanol-rich dark chocolate administration on (1) flow-mediated dilation and wave reflections; (2) blood pressure, endothelin-1 and oxidative stress, before and after oral glucose tolerance test (OGTT 1 Atherosclerotic pathology is a common sequela to T2DM, with macrovascular and microvascular diseases being among the leading causes of morbidity and mortality in patients with T2DM.2 Even after adjustment for conventional risk factors, individuals with T2DM exhibit a 2-to 4-fold increased risk of mortality in comparison with individuals without diabetes.3 Thus, several investigations have been directed to the potential adverse effects of hyperglycemia on the arterial wall. Observational data reveal high blood glucose concentrations are a risk factor for mortality, even in nondiabetic individuals. 4 Postprandial hyperglycemia has also been implicated in the development of cardiovascular disease. Elevated postprandial glucose may have a direct toxic effect on the vascular endothelium mediated by oxidative stress, independent of other cardiovascular risk factors, such as hyperlipidemia.2,5 A highcarbohydrate meal has been described to increase oxidative stress and favor proinflammatory effects.
5Several in vivo studies have found impaired nitric oxide (NO)-mediated endothelial function during acute episodes of hyperglycemia.6-10 NO is a key endothelium-derived relaxing factor and plays a pivotal role in the maintenance of basal vascular tone and vascular responses to dilative stimuli. [11][12][13] NO acts to negate the actions of endothelium-derived contracting factors such as angiotensin II and endothelin-1 (ET-1), as well as inhibit platelet aggregability 11-13 and endothelial activation.11-13 Therefore, reduced NO bioavailability may contribute to the onset and progression of endothelial dysfunction, including impaired vasodilative and increased adhesive properties, leading to atherogenesis.11-13 Additionally, endothelium-derived NO may act to regulate arterial stiffness and wave reflec-