Hydrogen sulfide downregulates colonic afferent sensitivity by a nitric oxide synthase-dependent mechanism in mice

Neurogastroenterology and Motility : the Official Journal of the European Gastrointestinal Motility Society
Xiaomeng XuChuanyong Liu

Abstract

The effect of hydrogen sulfide (H2 S) on visceral nociception is elusive. The conflicting evidence of its pro- and antinociceptive effects raises a series of questions with respect to the effect of H2 S on colonic afferent activity and the underlying mechanism, which was further elucidated in this study. Colonic mesenteric afferent nerve spikes of normal male C57BL/6J mice, Cbs+/- mice, and Wistar rats were recorded in vitro. The abdominal withdrawal reflex (AWR) induced by colorectal distension (CRD) was evaluated in Cbs+/- mice and WT littermates. Sodium hydrosulfide (NaHS) significantly decreased colonic afferent spontaneous discharge, chemosensitivity to bradykinin, mechanosensitivity to ramp distention, and intraluminal pressure in mice. Reducing the relaxant action of NaHS on intestinal smooth muscle using the nonspecific K+ channel blocker TEA (10 mmol/L) did not block the inhibition of NaHS on afferent nerve activity. The inhibitory effects of NaHS (0.5 mmol/L) on colonic afferent sensitivity were largely eliminated by the pretreatment with nonspecific NOS inhibitor NG -Methyl-l-arginine acetate salt (1 mmol/L), the specific nNOS inhibitor NPLA (1 μmol/L), or N-type Ca2+ channel blocker ω-conotoxin GVIA (1 μmol/L). Comp...Continue Reading

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Citations

Sep 29, 2020·Frontiers in Cellular Neuroscience·Kseniia KorolevaGuzel Sitdikova

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