The gaseous mediator, hydrogen sulphide, inhibits <i>in vitro</i> motor patterns in the human, rat and mouse colon and jejunum

Hydrogen sulphide (H2S) has been recently proposed as a transmitter in the brain and peripheral tissues. Its role in the gastrointestinal tract is still unknown despite some data which suggest an involvement mediating smooth muscle relaxation. The aim of this study was to investigate the effect of this gas on intestinal segments from mouse jejunum and colon, and muscular strips from the human and rat colon. In isolated segments of mouse colon and jejunum, bath applied sodium hydrogen sulphide (NaHS) (a H2S donor) caused a concentration-dependent inhibition of spontaneous motor complexes (MCs) (IC(50) 121 micromol L(-1) in the colon and 150 micromol L(-1) in the jejunum). This inhibitory effect of NaHS on MCs was (i) unaffected by tetrodotoxin (TTX), capsaicin, pyridoxal-phosphate-6-azophenyl-2',4'-disulfonate and N-nitro-L-arginine suggesting a non-neural effect and (ii) significantly reduced by apamin 3 micromol L(-1). NaHS concentration-dependently inhibited the spontaneous motility in strips from human colon (IC(50) 261 micromol L(-1)) and rat colon (IC(50) 31 micromol L(-1)). The inhibitory effect of NaHS on colonic strips was (i) unaffected by the neural blocker TTX (1 micromol L(-1)) with IC(50) 183 micromol L(-1) for the human colon and of 26 micromol L(-1) for the rat colon and (ii) significantly reduced by glybenclamide (10 micromol L(-1)), apamin (3 micromol L(-1)) and TEA (10 mmol L(-1)) with IC(50) values of 2464, 1307 and 2421 micromol L(-1) for human strips, and 80, 167 and 674 micromol L(-1) for rat strips respectively. We conclude that H2S strongly inhibits in vitro intestinal and colonic motor patterns. This effect appears to be critically dependent on K channels particularly apamin-sensitive SK channels and glybenclamide-sensitive K (ATP) channels.