| First Author | Kim CD | Year | 1999 |
| Journal | Am J Physiol | Volume | 277 |
| Issue | 2 Pt 1 | Pages | G280-4 |
| PubMed ID | 10444441 | Mgi Jnum | J:56948 |
| Mgi Id | MGI:1342926 | Doi | 10.1152/ajpgi.1999.277.2.G280 |
| Citation | Kim CD, et al. (1999) Neuronal NOS provides nitrergic inhibitory neurotransmitter in mouse lower esophageal sphincter. Am J Physiol 277(2 Pt 1):G280-4 |
| abstractText | 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(omega)-nitro-L-arginine methyl ester (100 microM) 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. |
