Effect of galanin and galanin antagonists on peristalsis in esophageal smooth muscle in the opossum

Citation
S. Yamato et al., Effect of galanin and galanin antagonists on peristalsis in esophageal smooth muscle in the opossum, AM J P-GAST, 279(4), 2000, pp. G719-G725
Citations number
29
Categorie Soggetti
da verificare
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
ISSN journal
01931857 → ACNP
Volume
279
Issue
4
Year of publication
2000
Pages
G719 - G725
Database
ISI
SICI code
0193-1857(200010)279:4<G719:EOGAGA>2.0.ZU;2-3
Abstract
Galanin, a neuropeptide that is widely distributed in the esophageal nerves , is known to exert a neuromodulatory action in the gut. These studies exam ined the effect of galanin and galanin antagonists on esophageal peristalsi s in anesthetized opossums in vivo. Intraluminal esophageal pressures were recorded at 1, 3, 5, 7, and 9 cm above the lower esophageal sphincter. Esop hageal peristaltic contractions were induced by swallow and short- (1-s) an d long-train (10-s) vagal stimulation (VS). Galanin (1 nmol/kg) inhibited t he amplitude of swallow-induced peristaltic contractions and increased peri staltic velocity by enlarging the latency periods in the upper part of the esophagus and reducing them in the lower part. Galinin nearly abolished eso phageal contractions caused by short- train VS at 5 Hz and inhibited the co ntractions at 10 Hz. Galanin increased latency periods induced by short- tr ain VS with little change in the velocity of peristalsis and reduced the am plitude of both A (cholinergic) and B (noncholinergic) contractions due to long-train VS. However, the decrease in amplitude of B contractions was mor e marked. Galantide (3 nmol/kg) antagonized the inhibitory action of exogen ous galanin on esophageal contractions elicited by short- train VS, but by itself galantide had no significant effect on esophageal contractions. In c onclusion, exogenous galanin inhibits the amplitude of swallow-induced peri staltic contractions and converts them into nonperistaltic contractions by inhibiting both the cholinergic and noncholinergic components.