title: Hydrogen sulphide and pain.
abstract: Physiopathological mechanisms and treatment of pain remain a significant challenge. In the last decade, the gasotransmitter hydrogen sulphide (H(2)S) has received wide attention for its ability to act as a multilevel regulatory molecule in a variety of biologic functions in mammals including modulation of pain processing. Results from preclinical models of pain, including experimentally-induced somatic, neurophatic and visceral pain have provided non univocal finding and, depending on the model, H(2)S has been reported to exert either pronociceptive and antinociceptive effects. Several biochemical explanations might account for these differences: thus, H(2)S-induced pronociception appears linked to activation of T-type Ca(2+) channels while analgesia is due to K(ATP) channels opening. Moreover, local administration of H(2)S causes pain and, in contrast, systemic H(2)S administration results into antinociception. In the view of possibility to use H(2)S-realising drugs or compounds that block H(2)S synthesis for pain treatment, additional studies are needed to exploit the therapeutic potential of H(2)S in pain signalling.
authors.affiliation: S.C. di Gastroenterologia ed Epatologia, Azienda Ospedaliera di Perugia, 06122, Perugia, Italy. eleonora.distrutti@unipg.it
authors.forename: Elenora
authors.initials: E
authors.lastname: Distrutti
mesh_terms: D000700:Analgesics / Q000494:pharmacology*; D000818:Animals; D020747:Calcium Channels, T-Type / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D006862:Hydrogen Sulfide / Q000378:metabolism*; D054086:KATP Channels / Q000378:metabolism; D009437:Neuralgia / Q000188:drug therapy / Q000503:physiopathology; D010146:Pain / Q000188:drug therapy / Q000503:physiopathology*
chemical_list: D000700:Analgesics; D020747:Calcium Channels, T-Type; D054086:KATP Channels; D006862:Hydrogen Sulfide