Participation of nitric oxide in the nicotine-induced relaxation of the cat lower esophageal sphincter.

The participation of nitric oxide in the relaxation of the cat lower esophageal sphincter muscle strip in response to electrical field stimulation or administration of nicotine was studied. The nicotine-induced relaxation was mediated via a neuronal pathway, since it was inhibited by administration of hexamethonium or tetrodotoxin. Inhibition of nitric oxide biosynthesis by N-nitro-L-arginine decreased the relaxation induced by nicotine (50 microM) or field stimulation. With the maximal concentration of N-nitro-L-arginine (1 mM) electrical field stimulation-induced relaxation was abolished, while nicotine-induced relaxation decreased by 70%. L-Arginine (1 mM) partly restored this relaxation. Desensitization of P2x receptors by alpha, beta methylene-adenosine 5-triphosphate (alpha, beta-m-ATP) did not change the relaxation induced by either electrical field stimulation or administration of nicotine. It is therefore suggested that the field stimulation-induced relaxation is mediated by the release of nitric oxide, but in the nicotine-produced relaxation is only partly due to nitric oxide, other factor(s) might be also be involved.