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1 Center for Swallowing and Motility Disorders,
To identify the
enzymatic source of nitric oxide (NO) in the lower esophageal sphincter
(LES), studies were performed in wild-type and genetically engineered
endothelial nitric oxide synthase [eNOS(
)] and neuronal NOS
[nNOS()] mice. Under nonadrenergic noncholinergic (NANC)
conditions, LES ring preparations developed spontaneous tone in all
animals. In the wild-type mice, electrical field stimulation produced
frequency-dependent intrastimulus relaxation and a poststimulus rebound
contraction. NOS inhibitor
N
-nitro-L-arginine methyl ester
(100 µM) abolished intrastimulus relaxation and rebound contraction.
In nNOS() mice, both the intrastimulus relaxation and rebound
contraction were absent. However, in eNOS() mice there was no
significant difference in either the relaxation or rebound contraction
from the wild-type animal. Both nNOS() and eNOS() tissues
showed concentration-dependent relaxation to NO donor
diethylenetriamine-NO and there was no difference in the sensitivity to
the NO donor in nNOS(), eNOS(), or wild-type animals.
These results indicate that in mouse LES, nNOS rather than eNOS is the
enzymatic source of the NO that mediates NANC relaxation and rebound contraction.
nitric oxide; nonadrenergic noncholinergic neurotransmission; endothelial nitric oxide synthase lacking mutant mice
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