Hydrogen sulphide as a signalling molecule regulating physiopathological processes in gastrointestinal motility

M. Jimenez, V. Gil, M. Martinez-Cutillas, N. Mañé, D. Gallego

Research output: Contribution to journalReview articleResearchpeer-review

11 Citations (Scopus)

Abstract

© 2017 The British Pharmacological Society The biology of H2S is a still developing area of research and several biological functions have been recently attributed to this gaseous molecule in many physiological systems, including the cardiovascular, urogenital, respiratory, digestive and central nervous system (CNS). H2S exerts anti-inflammatory effects and can be considered an endogenous mediator with potential effects on gastrointestinal motility. During the last few years, we have investigated the role of H2S as a regulator of gastrointestinal motility using both animal and human tissues. The aim of the present work is to review published data regarding the potential role of H2S as a signalling molecule regulating physiopathological processes in gastrointestinal motor function. H2S is endogenously produced by defined enzymic pathways in different cell types of the intestinal wall including neurons and smooth muscle. Inhibition of H2S biosynthesis increases motility and H2S donors cause smooth muscle relaxation and inhibition of propulsive motor patterns. Impaired H2S production has been described in animal models with gastrointestinal motor dysfunction. The mechanism(s) of action underlying these effects may include several ion channels, although no specific receptor has been identified. At this time, even though there is much experimental evidence for H2S as a modulator of gastrointestinal motility, we still do not have conclusive experimental evidence to definitively propose H2S as an inhibitory neurotransmitter in the gastrointestinal tract, causing nerve-mediated relaxation.
Original languageEnglish
Pages (from-to)2805-2817
JournalBritish Journal of Pharmacology
Volume174
Issue number17
DOIs
Publication statusPublished - 1 Jan 2017

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