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Am J Physiol Gastrointest Liver Physiol 277: G280-G284, 1999;
0193-1857/99 $5.00
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Vol. 277, Issue 2, G280-G284, August 1999

Neuronal NOS provides nitrergic inhibitory neurotransmitter in mouse lower esophageal sphincter

Chi Dae Kim1, Raj K. Goyal1, and Hiroshi Mashimo1,2

1 Center for Swallowing and Motility Disorders, Brockton/West Roxbury Veterans Affairs Medical Center, and 2 Gastrointestinal Unit, Massachusetts General Hospital, and Harvard Medical School, Boston, Massachusetts 02132

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 Nomega -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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