Physiopathological mechanisms and treatment of pain remain a significant challenge. In the last decade, the gasotransmitter hydrogen sulphide (H2S) 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, H2S has been reported to exert either pronociceptive and antinociceptive effects. Several biochemical explanations might account for these differences: thus, H2S-induced pronociception appears linked to activation of T-type Ca2+ channels while analgesia is due to KATP channels opening. Moreover, local administration of H2S causes pain and, in contrast, systemic H2S administration results into antinociception. In the view of possibility to use H2S-realising drugs or compounds that block H2S synthesis for pain treatment, additional studies are needed to exploit the therapeutic potential of H2S in pain signalling.
Keywords: Antinociception, gasotransmitters, hyperalgesia, irritable bowel syndrome, KATP channels, μ opioid receptors, Hydrogen sulphide, μ-opioid receptors, T-type Ca2+ channels, NO-cGMP pathway
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