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Arterial hypertension constitutes a central factor in the pathogenesis of stroke. We examined endothelial function of the retinal vasculature as a model of the cerebral circulation.Thirty-eight young subjects (19 hypertensive and 19 normotensive) were treated with the AT1-receptor blocker candesartan cilexetil and placebo, each over 7 days. Retinal capillary flow and blood flow velocity in the central retinal artery were assessed with scanning laser Doppler flowmetry and pulsed Doppler ultrasound, respectively. NG-mono-methyl-L-arginine (L-NMMA) was infused to inhibit nitric oxide (NO) synthesis. Diffuse luminance flicker was applied to stimulate NO release.In normotensive subjects, L-NMMA decreased retinal capillary flow by 8.2%±13% (P < 0.05) and flickering light increased mean blood flow velocity in the central retinal artery by 19%±29% (P < 0.01). In contrast, no significant change to these provocative tests was seen in hypertensive subjects. Treatment with candesartan cilexetil restored a normal pattern of reactivity in retinal capillaries (L-NMMA: decrease in perfusion by 10%±17%, P < 0.05) and the central retinal artery (flicker: increase in mean blood flow velocity by 42%±31%, P < 0.001) in hypertensive patients.Endothelial function of the retinal vasculature is impaired in early essential hypertension but can be improved by AT1-receptor blockade.