

Author: Tamai Kazushi Suzuki Hikaru Shirai Shoichiro Ogura Yuichiro
Publisher: Informa Healthcare
ISSN: 0271-3683
Source: Current Eye Research, Vol.19, Iss.2, 1999-08, pp. : 182-187
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Abstract
PURPOSE. To assess the roles of endothelium-derived vasodilators and K + channels on metabolic ischemia-induced vasodilation from diameter changes in choroidal arterioles of the guinea-pig. METHODS. The choroid was isolated from the guinea-pig eye-ball, pinned flat on a silicone rubber plate, and superfused with oxygenated warmed (35°C) Krebs solution. Diameters of choroidal arterioles were measured using video microscopy and a computer program for analysis. Vasodilatory effects were examined after the choroid was exposed to glucose-free/NaCN solutions for 10 minutes. The effects of N?-nitro-L-arginine (nitroarginine), indomethacin, and K + channel inhibitors (glibenclamide [Glib] and charybdotoxin [ChTX]) on ischemic vasodilation were assessed. RESULTS. Reversible vasodilation was observed when the choroid was exposed to glucose-free/NaCN (10 -3 M) solutions. Nitroarginine (10 -4 M), Glib (2×10 -5 M) and ChTX (10 -7 M) significantly inhibited glucose-free/NaCN (10 -3 M)-induced vasodilation by 47%, 62%, and 24%, respectively. No significant inhibitory effect was observed with indomethacin (10 -5 M). Simultaneous application of Glib and ChTX reduced vasodilation by 77%. When Glib and ChTX were added together to nitroarginine, dilation was reduced by 86%. With high K + ([K]o = 47.2 mM) Krebs solution, ischemia caused a slight vasodilation (11%), which was significantly inhibited by nitroarginine. CONCLUSIONS. In guinea-pig choroidal arterioles, glucose-free/ NaCN-induced ischemic vasodilation was mainly mediated by NO and K ATP channels. A part of NO-mediated vasodilation was induced independent of the opening of K + channels.
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