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Nitric oxide regulates retinal vascular tone in humans

Departments of ¹Clinical Pharmacology and ²Ophthalmology and ³Institute of Medical Physics, University of Vienna Medical School, Vienna A-1090, Austria; and ⁴Institut de Recherche en Ophthalmologie, CH-1950 Sion, Switzerland

Submitted 10 February 2003 ; accepted in final form 4 May 2003

The purpose of the present study was to investigate the contribution of basal nitric oxide (NO) on retinal vascular tone in humans. In addition, we set out to elucidate the role of NO in flicker-induced retinal vasodilation in humans. Twelve healthy young subjects were studied in a three-way crossover design. Subjects received an intravenous infusion of either placebo or N^G-monomethyl-L-arginine (L-NMMA; 3 or 6 mg/kg over 5 min), an inhibitor of NO synthase. Thereafter, diffuse luminance flicker was consecutively performed for 16, 32, and 64 s at a frequency of 8 Hz. The effect of L-NMMA on retinal arterial and venous diameter was assessed under resting conditions and during the hyperemic flicker response. Retinal vessel diameter was measured with a Zeiss retinal vessel analyzer. L-NMMA significantly reduced arterial diameter (3 mg/kg: –2%; 6 mg/kg: –4%, P < 0.001) and venous diameter (3 mg/kg: –5%; 6 mg/kg: –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 s, 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.

retinal vessel diameter; human retinal blood flow; retinal vessel analyzer; luminance flicker

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