Impaired endothelial function of the retinal vasculature in hypertensive patients

Background and Purpose-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. Methods-Thirty-eight young subjects (19 hypertensive and 19 normotensive) were treated with the AT(1)-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. N-G-mono-methyl-L-arginine (L-NMMA) was infused to inhibit nitric oxide (NO) synthesis. Diffuse luminance flicker was applied to stimulate NO release. Results-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. Conclusions-Endothelial function of the retinal vasculature is impaired in early essential hypertension but can be improved by AT(1)-receptor blockade.