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Abstract #5442 Published in IGR 1-2
Effect of K+ channel blockers on acetylcholine-induced vasodilatation in guinea-pig choroid
Tamai K; Suzuki H; Hashitani H; Shirai S; Ogura YExperimental Eye Research 1999; 69: 85-90
The purpose of this study is to clarify which K+ channels contribute to the acetylcholine (ACh)-induced vasodilatation from the diameter changes in arterioles of the guinea-pig choroid. The choroid was isolated from the guinea-pig eyeball, pinned flat on a silicone rubber plate, and superfused with warmed oxygenated (35?C) Krebs solution. Diameters of choroidal arterioles were measured using video microscopy and a computer program for analysis. The effects of K+ channel inhibitors (glibenclamide, tetraethylammonium (TEA), apamin and charybdotoxin (ChTX)) on the ACh-induced vasodilatation were examined in arterioles which had been constricted by either norepinephrine (NE) or high K+ solution. In NE (10-5 m)-constricted arterioles, the combination of nitroarginine (10-4 m) and indomethacin (10-5 m) reduced ACh (10-6 m)-induced vasodilatation by 24%. When high K+ solution was used to constrict the arterioles, ACh-induced vasodilatation was abolished by nitroarginine and indomethacin. In the presence of nitroarginine and indomethacin, the ACh-induced dilatation of NE-constricted arterioles was attenuated by TEA (10-3 m), apamin (10-7 m), and ChTX (10-7 m), but not by glibenclamide (2x10-5 m). Simultaneous application of apamin and ChTX inhibited the ACh (10-6 m)-induced dilatation by 85%. In arterioles of guinea-pig choroid, nitric oxide and prostacyclin are not main mediators in ACh-induced vasodilatation. Simultaneous activation of a set of Ca2+ sensitive K+ channels may take most part of ACh-induced vasodilatation.
K. Tamai, Department of Ophthalmology, Nagoya City University Medical School, Nagoya; Japan
Classification:
11.7 Treatment of bloodflow (Part of: 11 Medical treatment)
