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Submitted on December 4, 2003
From Departments of Nephrology (C.D., S.O., K.F.H., R.E.S.) and Ophthalmology (G.M., J.H.), University of Erlangen-Nürnberg, Erlangen, Germany. * To whom correspondence should be addressed. E-mail: roland.schmieder{at}rzmail.uni-erlangen.de.
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. NG-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.
Revised on January 12, 2004
Accepted on February 10, 2004
Impaired Endothelial Function of the Retinal Vasculature in Hypertensive Patients
Christian Delles MD;
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