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Departments of 1 Physiology and 2 Pharmacology, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, United Kingdom
In rat
mesenteric artery, endothelium-derived hyperpolarizing factor (EDHF) is
blocked by a combination of apamin and charybdotoxin (ChTX). The site of action of these toxins has not been
established. We compared the effects of ChTX and apamin applied
selectively to the endothelium and to the smooth muscle. In
isometrically mounted arteries, ACh (0.01-10 µm), in the
presence of indomethacin (2.8 µM) and
N
-nitro-L-arginine
methyl ester (L-NAME) (100 µM), concentration dependently relaxed phenylephrine (PE)-stimulated
tone (EC50 50 nM;
n = 10). Apamin (50 nM) and ChTX (50 nM) abolished this relaxation (n = 5).
In pressurized arteries, ACh (10 µM), applied intraluminally in the
presence of indomethacin (2.8 µM) and
L-NAME (100 µM), dilated both
PE-stimulated (0.3-0.5 µM; n = 5) and myogenic tone (n = 3). Apamin
(50 nM ) and ChTX (50 nM) applied intraluminally abolished ACh-induced
dilatations. Bath superperfusion of apamin and ChTX did not affect
ACh-induced dilatations of either PE-stimulated (n = 5) or myogenic tone
(n = 3). This is the first
demonstration that ChTX and apamin act selectively on the endothelium
to block EDHF-mediated relaxation.
smooth muscle; potassium; acetylcholine; endothelium-derived hyperpolarizing factor
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