Colonic Hydrogen Sulfide–Induced Visceral Pain and Referred Hyperalgesia Involve Activation of Both Cav3.2 and TRPA1 Channels in Mice

Journal of Pharmacological Sciences

Atsufumi Kawabata¹  Maho Tsubota-Matsunami¹  Fumiko Sekiguchi¹  Yasumasa Okawa¹  Yumi Noguchi¹ 

[1] Division of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, Japan

关键词: hydrogen sulfide;    T-type calcium channel;    TRPA1;   

DOI  :  10.1254/jphs.12086SC

学科分类：药学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(14)Cited-By(8)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 H2S-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 knockdown 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.

【 授权许可】

Unknown