Hydrogen sulphide-mediated vasodilatation involves the release of neurotransmitters from sensory nerves in pressurized mesenteric small arteries isolated from rats.

摘要: Background and Purpose Hydrogen sulphide (H2S) is a gas that has recently been shown to have biological activity. In the majority of blood vessels studied so far, H2S cause vasorelaxation, although contractile responses reported. present study, we made pharmacological assessment effects in mesenteric small arteries isolated from rats. Experimental Approach Rat were using pressure myography. pressurised arteries, obtained donor, sodium hydrogen (NaHS), absence presence NOS inhibitor L-NAME, raised extracellular potassium, KATP channel glibenclamide, Cl– blockers DIDS, NPPB A9C, TRPV1 receptor desensitizing agent, capsaicin, CGRP antagonist, olcegepant, blocker capsazepine TRPA1 HC-030031. Key Results NaHS produced vasodilator response rat held at 90 mmHg. Responses NaHS not reproducible. Neither, glibenclamide nor, L-NAME inhibited NaHS. DIDS abolished NaHS, but these unaffected by chloride blockers, A9C. attenuated after capsaicin pre-treatment, antagonist an channels. Conclusions Implications In mesentery, caused vasodilatation. This was reproducible vitro, since it mediated release sensory neurotransmitters capsaicin-like action. H2S-induced activation channels.