N. Kortezova et al., PARTICIPATION OF NITRIC-OXIDE IN THE NICOTINE-INDUCED RELAXATION OF THE CAT LOWER ESOPHAGEAL SPHINCTER, Journal of the autonomic nervous system, 50(1), 1994, pp. 73-78
The participation of nitric oxide in the relaxation of the cat lower e
sophageal sphincter muscle strip in response to electrical field stimu
lation or administration of nicotine was studied. The nicotine-induced
relaxation was mediated via a neuronal pathway, since it was inhibite
d by administration of hexamethonium or tetrodotoxini Inhibition of ni
tric oxide biosynthesis by N-nitro-L-arginine decreased the relaxation
induced by nicotine (50 mu M) or field stimulation. With the maximal
concentration of N-nitro-L-arginine (1 mM) electrical field stimulatio
n-induced relaxation was abolished, while nicotine-induced relaxation
decreased by 70%. L-Arginine (1 mM) partly restored this relaxation. D
esensitization of P-2x receptors by alpha,beta methylene-adenosine 5-t
riphosphate (alpha,beta(o)-m-ATP) did not change the relaxation induce
d by either electrical field stimulation or administration of nicotine
. It is therefore suggested that the field stimulation-induced relaxat
ion is mediated by the release of nitric oxide, but in the nicotine-pr
oduced relaxation is only partly due to nitric oxide, other factor(s)
might be also be involved.