Mechanisms of action of the gasotransmitter hydrogen sulfide in modulating contractile activity of longitudinal muscle of rat ileum.

AIM: This study aims to determine mechanisms of action of the gasotransmitter hydrogen sulfide (H(2)S) on contractile activity in longitudinal muscle of rat ileum.
METHODS: Ileal longitudinal muscle strips were prepared to measure isometric contractions. Effects of sodium hydrosulfide (NaHS), a donor of H(2)S, were evaluated on spontaneous contractile activity and after enhanced contractile activity with bethanechol. L-cysteine was evaluated as a potential endogenous donor of H(2)S. We evaluated involvement of extrinsic nerves, enteric nervous system, visceral afferent nerves, nitric oxide, and K(ATP)(+) channel and K(Ca)(+) channel activity on the action of H(2)S using non-adrenergic/non-cholinergic conditions, tetrodotoxin, capsaicin, L-N(G)-nitro arginine (L-NNA), glibenclamide, and apamin, respectively, as well as electrical field stimulation. RESULT: NaHS dose-dependently and reversibly inhibited spontaneous and bethanechol-stimulated contractile activity (p < 0.05). L-cysteine had no inhibitory effect. Non-adrenergic/non-cholinergic conditions, tetrodotoxin, capsaicin, L-NNA, glibenclamide, or apamin had no major effect on total contractile activity by NaHS, although both tetrodotoxin and apamin decreased the frequency of bethanechol-enhanced contractile activity (p < 0.05). We could not demonstrate H(2)S release by electrical field stimulation but did show that inhibition of cystathionine β synthase, an endogenous source of H(2)S, augmented the inhibitory effect of low-frequency electrical field stimulation.
CONCLUSION: H(2)S inhibits contractile activity of ileal longitudinal muscle dose-dependently but not through pathways mediated by the extrinsic or enteric nervous system, visceral afferent nerves, nitric oxide, K(ATP)(+) channels, or K(Ca)(+) channels.