Our findings are consistent with earlier observations and reinforce the essential role of SP, and its interaction with H2S. It must be noted, however, that with the usage of capsazepine, a synthetic competitive antagonist of TRPV1; our results provide the first pharmacological evidence that H2S provokes tachykinin-mediated neurogenic inflammatory responses involving SP in sepsis in a TRPV1-dependent manner. Here, TRPV1 is linked to Sepsis.