Impaired endothelial function of the retinal vasculature in hypertensive patients.

Author(s): Delles C, Michelson G, Harazny J, Oehmer S, Hilgers KF, Schmieder RE

Affiliation(s): Department of Nephrology, University of Erlangen-Nurnberg, Erlangen, Germany.

Publication date & source: 2004-06, Stroke., 35(6):1289-93. Epub 2004 Apr 8.

Publication type: Clinical Trial; Randomized Controlled Trial

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 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. N(G)-monomethyl-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 AT1-receptor blockade.