H2S and pain

Like nitric oxide and carbon monoxide, hydrogen sulfide (H2S) is now considered a novel gasotransmitter, playing extensive roles throughout the mammalian body including the CNS. H2S appears to have multiple target molecules including ATP-sensitive K+ channels and N-methyl-D-aspartate (NMDA) receptors. Our recent electrophysiological study has provided evidence that T-type Ca2+ channels are novel targets for H2S in neuronal cells. H2S sensitizes T-type Ca2+ channels most probably through redox modulation. Interestingly, intraplantar administration of H2S donor causes hyperalgesia in rats, an effect being blocked by mibefradil, an inhibitor of T-type Ca2+ channels. Inhibitors of an H2S-forming enzyme attenuate the inflammatory hyperalgesia induced by intraplantar administration of lipopolysaccharide. Roles for H2S in processing of visceral nociception are a little complex. H2S might play opposing roles in distinct models for visceral pain, being pro- and anti-nociceptive. Together, H2S could be a novel gasotransmitter for processing of somatic and visceral pain.