The purpose of this study is to clarify which K+ channels contribute to the
acetylcholine (ACh)-induced vasodilation from the diameter changes in arte
rioles of the guinea-pig choroid.
The choroid was isolated from the guinea-pig eyeball, pinned flat on a sili
cone rubber plate and superfused with warmed oxygenated (35 degrees C) Kreb
s solution. Diameters of choroidal arterioles were measured using video mic
roscopy and a computer program for analysis. The effects of K+ channel inhi
bitors (glibenclamide, tetraethylammonium [TEA], apamin and charybdotoxin [
ChTX]) on the ACh-induced vasodilation were examined in arterioles which ha
d 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 vasodila
tation by 24%. When high K+ solution was used to constrict the arterioles,
ACh-induced vasodilation was abolished by nitroarginine and indomethacin. I
n the presence of nitroarginine and indomethacin, the ACh-induced dilatatio
n of NE-constricted arterioles was attenuated by TEA (10(-3) M), apamin (10
(-7) M), and ChTX (10(-7) M) but not by glibenclamide (2 x 10(-5) M). Simul
taneous 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 vasodilation. Simultaneous activation of a se
t of Ca2+-sensitive K+ channels may take most part of ACh-induced vasodilat
ion. (C) 1999 Academic Press.