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Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226
Responses of
epicardial coronary arterioles to ACh were measured using stroboscopic
fluorescence microangiography in dogs (n = 38). ACh (0.1 and 0.5 µg · kg
1 · min1
ic) dilated small (<100 µm, 11 ± 2 and 19 ± 2%,
respectively) and large (>100 µm, 6 ± 3 and 13 ± 3%,
respectively) arterioles at baseline. Combined administration of
N
-monomethyl-L-arginine
(L-NMMA; 1.0 µmol/min ic) and indomethacin (10 mg/kg iv)
eliminated ACh-induced dilation in large coronary arterioles but only
partially attenuated that in small arterioles. Suffusion of a buffer
containing 60 mM KCl (high KCl) completely abolished cromakalim-induced
dilation in arterioles and in combination with L-NMMA plus
indomethacin completely blocked ACh-induced dilation in small
arterioles. This indicated that the vasodilation to ACh that persists
in small arterioles after administration of L-NMMA and
indomethacin is mediated via a hyperpolarizing factor. The ACh-induced
vasodilation remaining after L-NMMA and indomethacin was
completely blocked by the large-conductance potassium-channel antagonist iberiotoxin or by epicardial suffusion of miconazole or
metyrapone, inhibitors of cytochrome
P-450 enzymes. These observations are
consistent with the view that endothelium-derived hyperpolarizing factor (EDHF) is a product of cytochrome
P-450 enzymes and produces vasodilation by the opening of large-conductance potassium channels. We
conclude that ACh-induced dilation in large coronary arterioles is
mediated mainly by nitric oxide (NO), whereas, in small arterioles both
NO and EDHF mediate dilation to ACh. These data provide the first
direct evidence for an in vivo role of EDHF in small coronary arterioles.
coronary circulation; endothelium-dependent dilation; hyperpolarization; endothelium-derived hyperpolarizing factor
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