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

Abstract

Hydrogen sulphide (H 2 S) 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 H 2 S donor) caused a concentration-dependent inhibition of spontaneous motor complexes (MCs) (IC 50 121 lmol L human strips, and 80, 167 and 674 lmol L )1 for rat strips respectively. We conclude that H 2 S 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.

Synthesis of H2S in the Gastrointestinal Tract

“…Interestingly, H2S exhibited different effects on different colonic motility patterns, for example, NaHS inhibited rhythmic propulsive motor complexes (RPMCs) which is associated with outflow, but enhanced the amplitude of ripples which may be associated with promoting mixing. The inhibitory effect of NaHS on the colonic motility was reduced by KATP channel blocker and small conductance calcium-activated potassium channel (SKCa) blocker, which suggest that both KATP and SKCa channels are involved in the effect [45,50,51] .…”

“…Since glibenclamide and L-NAME, a nitric oxide synthase, did not affect the NaHS-induced inhibition, so that KATP channel and NO were not involved in the effect [49] . In the rat and human colon, NaHS also inhibited the colonic motility [45,50,51] . Interestingly, H2S exhibited different effects on different colonic motility patterns, for example, NaHS inhibited rhythmic propulsive motor complexes (RPMCs) which is associated with outflow, but enhanced the amplitude of ripples which may be associated with promoting mixing.…”

“…Gallego et al [45] demonstrated that NaHS inhibited the spontaneous contraction of the jejunal smooth muscle in mouse, which may be a direct effect on the smooth muscle cells because TTX had no significant effect on the NaHS-induced inhibition and in the TRPV1-/-animals the inhibitory effect still existed. Similarly, Sarr team [29,44] also found that NaHS inhibited both spontaneous and bethanechol stimulated contraction of the jejunal smooth muscle in Lewis rats.…”

“…In the mouse colon, it has demonstrated that NaHS inhibited the spontaneous and pre-contracted smooth muscle contraction in a dosedependent manner, which was not via neuronal pathway because both TTX and TRPV1 blocker capsazepine had no significant effects on the inhibition [45,49] . Since glibenclamide and L-NAME, a nitric oxide synthase, did not affect the NaHS-induced inhibition, so that KATP channel and NO were not involved in the effect [49] .…”

“…Different from the Wistar rats, in the Lewis rats and mouse jejunum, NaHS induced an inhibitory effect on the smooth muscle motility [29,44,45] . Gallego et al [45] demonstrated that NaHS inhibited the spontaneous contraction of the jejunal smooth muscle in mouse, which may be a direct effect on the smooth muscle cells because TTX had no significant effect on the NaHS-induced inhibition and in the TRPV1-/-animals the inhibitory effect still existed.…”