Electrophysiological, pharmacological and gene-knockdown studies have shown that hydrogen sulfide (H₂S) promotes pain or itch by enhancing Ca_v3.2 T-type Ca²⁺ channel activity. We thus examined the effect of Ca_v3.2 gene deletion on H₂S-dependent somatic or visceral pain and itch. In wild-type mice, intraplantar and intracolonic administration of Na₂S, an H₂S donor, caused somatic and colonic pain/hypersensitivity, respectively, and intradermal injection of Na₂S in the cheek evoked both pain and itch responses. These responses to Na₂S challenge disappeared in Ca_v3.2-KO mice. Ca_v3.2 deletion did not affect the partial sciatic nerve ligation (PSNL)-induced neuropathic allodynia in mice, but removed the anti-allodynic activity of T-type Ca²⁺ channel blockers. On the other hand, Ca_v3.2 deletion abolished endogenous H₂S-dependent bladder pain in mice with cyclophosphamide-induced cystitis, and the butyrate-induced colonic hypersensitivity in mice, models for bladder pain syndrome (BPS) and irritable bowel syndrome (IBS), respectively. Our data thus suggest that Ca_v3.2 plays a key role in exogenous H₂S-induced pain and itch, and in visceral pain signaling in BPS and IBS models, although unknown neuronal systems might compensate Ca_v3.2 deficiency in PSNL-induced neuropathy.