Colonic hydrogen sulfide-induced visceral pain and referred hyperalgesia involve activation of both Cav3.2 and TRPA1 channels in mice

Luminal hydrogen sulfide (h2s),a gasotransmitter,causes colonic pain / referred hyperalgesia in mice,most probably via activation of t-type ca2+ channels. here we analyzed the mechanisms for h 2s-induced facilitation of colonic pain signals. intracolonic administration of nahs,an h2s donor,evoked visceral pain-like nociceptive behavior and referred hyperalgesia in mice,an effect abolished by nnc 55-0396,a selective t-type ca2+-channel blocker,or by knock-down of cav3.2. ap18,a trpa1 blocker,also prevented the nahs-induced colonic pain and referred hyperalgesia. these findings demonstrate that h2s-induced colonic pain and referred hyperalgesia require activation of both cav3.2 and trpa1 channels in mice. © the japanese pharmacological society.