Colonic hydrogen sulfide-induced visceral pain and referred hyperalgesia involve activation of both Ca(v)3.2 and TRPA1 channels in mice.

Abstract

Luminal hydrogen sulfide (H(2)S), a gasotransmitter, causes colonic pain / referred hyperalgesia in mice, most probably via activation of T-type Ca(2+) channels. Here we analyzed the mechanisms for H(2)S-induced facilitation of colonic pain signals. Intracolonic administration of NaHS, an H(2)S donor, evoked visceral pain-like nociceptive behavior and referred hyperalgesia in mice, an effect abolished by NNC 55-0396, a selective T-type Ca(2+)-channel blocker, or by knockdown of Ca(v)3.2. AP18, a TRPA1 blocker, also prevented the NaHS-induced colonic pain and referred hyperalgesia. These findings demonstrate that H(2)S-induced colonic pain and referred hyperalgesia require activation of both Ca(v)3.2 and TRPA1 channels in mice.

• Authors: Maho Tsubota-Matsunami, Yumi Noguchi, Yasumasa Okawa, Fumiko Sekiguchi, Atsufumi Kawabata
• Journal: Journal of pharmacological sciences (J Pharmacol Sci) Vol. 119 Issue 3 Pg. 293-6 ( 2012) ISSN: 1347-8648 [Electronic] Japan
• PMID: 22785020 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Benzimidazoles
• Cacna1h protein, mouse
• Calcium Channels, T-Type
• Cyclopropanes
• Naphthalenes
• Sulfides
• TRPA1 Cation Channel
• Transient Receptor Potential Channels
• Trpa1 protein, mouse
• NNC 55-0396
• sodium bisulfide
• Hydrogen Sulfide

Topics

• Animals
• Benzimidazoles (pharmacology)
• Calcium Channels, T-Type (metabolism)
• Cyclopropanes (pharmacology)
• Female
• Hydrogen Sulfide (toxicity)
• Hyperalgesia (chemically induced, metabolism)
• Mice
• Naphthalenes (pharmacology)
• Nociceptors (metabolism)
• Sulfides (pharmacology)
• TRPA1 Cation Channel
• Transient Receptor Potential Channels (metabolism)
• Visceral Pain (chemically induced, metabolism)