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These results are very important in exploring the mechanism of physiological accommodation and accommodation disorder.<\/jats:p>\n<\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec><jats:sec><jats:label\/><jats:p>Hydrogen sulphide (H<jats:sub>2<\/jats:sub>S) is considered a new gasotransmitter, along with NO and CO. It was recently confirmed that H<jats:sub>2<\/jats:sub>S and NO play important roles in the regulation of gastrointestinal smooth muscle tension. The present study was designed to elucidate the interactions between H<jats:sub>2<\/jats:sub>S and NO with respect to the regulation of gastric fundus smooth muscle tension using Western blotting, physiological and electrochemical techniques. Real\u2010time H<jats:sub>2<\/jats:sub>S and NO generation was detected in gastric smooth muscle tissue. NaHS, an H<jats:sub>2<\/jats:sub>S donor, enhanced fundus smooth muscle tension, whereas SNP, an NO donor, decreased fundus smooth muscle tension in a dose\u2010dependent manner. NaHS\u2010induced increases in fundus smooth muscle tension were suppressed by <jats:sc>l<\/jats:sc>\u2010NAME, an NO synthase inhibitor. Aminooxyacetic acid (AOAA), a cystathionine \u03b2\u2010synthase inhibitor, exerted inhibitory effects on fundus smooth muscle tension; these effects were also suppressed by <jats:sc>l<\/jats:sc>\u2010NAME. Real\u2010time NO generation was significantly potentiated by AOAA. Endothelial nitric oxide synthase (eNOS) phosphorylation at serine 1177 and Akt phosphorylation at serine\u00a0308 and threonine\u00a0473 were significantly inhibited by NaHS. LY294002, a phosphoinositide 3\u2010kinase inhibitor, blocked these NaHS\u2010mediated effects. However, eNOS phosphorylation at serine\u00a01177 and Akt phosphorylation at serine\u00a0308 and threonine\u00a0473 were significantly potentiated by AOAA. Cystathionine \u03b2\u2010synthase siRNA interference significantly increased eNOS phosphorylation at serine 1177 and Akt phosphorylation at serine 308 and threonine 473. Cystathionine \u03b2\u2010synthase siRNA interference also increased total eNOS protein expression levels but did not significantly change total Akt kinase protein expression levels. These results suggest that H<jats:sub>2<\/jats:sub>S\u2010induced enhancement of gastric fundus tension is mediated by inhibition of NO generation through the phosphoinositide 3\u2010kinase\/Akt pathway.<\/jats:p><\/jats:sec>","DOI":"10.1113\/ep086288","type":"journal-article","created":{"date-parts":[[2017,4,6]],"date-time":"2017-04-06T16:52:03Z","timestamp":1491497523000},"page":"779-790","source":"Crossref","is-referenced-by-count":4,"title":["H<sub>2<\/sub>S\u2010induced gastric fundus smooth muscle tension potentiation is mediated by the phosphoinositide 3\u2010kinase\/Akt\/endothelial nitric oxide synthase pathway"],"prefix":"10.1113","volume":"102","author":[{"given":"Xiang\u2010Min","family":"Meng","sequence":"first","affiliation":[{"name":"Department of Physiology, College of Basic Medicine Shanghai Jiao Tong University School of Medicine  280 South Chongqing Road Shanghai 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