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1 Department of Clinical Pharmacology, University of Vienna Medical School, Vienna, Austria; Department of Ophthalmology, University of Vienna Medical School, Vienna, Austria
2 Department of Ophthalmology, University of Vienna Medical School, Vienna, Austria
3 Institut de Recherche en Ophthalmologie, Sion, Switzerland
4 Department of Clinical Pharmacology, University of Vienna Medical School, Vienna, Austria; Institute of Medical Physics, University of Vienna Medical School, Vienna, Austria
* To whom correspondence should be addressed. E-mail: leopold.schmetterer{at}univie.ac.at.
The purpose of the present study was to investigate the contribution of basal nitric oxide (NO) on retinal vascular tone in man. In addition, we set out to elucidate the role of NO in flicker-induced retinal vasodilation in man. 12 healthy young subjects were studied in a three way cross-over design. Subjects received intravenous infusion of either placebo or NG-monomethyl-L-arginine (L-NMMA; 3 mg.kg-1 or 6 mg.kg-1 over 5 minutes), an inhibitor of NO synthase. Thereafter diffuse luminance flicker was consecutively performed for 16, 32 and 64 seconds at a frequency of 8 Hz. The effect of L-NMMA on retinal arterial and venous diameter was assessed under resting conditions and during hyperemic flicker response. Retinal vessel diameter was measured with the Zeiss retinal vessel analyzer. L-NMMA significantly reduced arterial (3 mg.kg-1: -2%, 6 mg.kg-1: -4%, P < 0.001) and venous diameter (3 mg.kg-1: -5%, 6 mg.kg-1: -8%, P < 0.001). After placebo infusion flicker induced a significant increase in retinal vessel diameter (P < 0.001). At a flicker duration of 64 seconds arterial diameter increased by 4% and venous diameter increased by 3%. L-NMMA did not abolish these hyperemic responses, but blunted venous vasodilation (P = 0.017) and arterial vasodilation (P = 0.02) in response to flicker stimulation. Our data indicate that NO contributes to basal retinal vascular tone in humans. In addition, NO appears to play a role in flicker-induced vasodilation of the human retinal vasculature.
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