Aim: Our aim was to determine mechanisms of action of the gasotransmitter hydrogen sulfide (H 2S) on contractile activity in circular muscle of rat jejunum. Methods: Jejunal circular muscle strips were prepared to measure isometric contractions. Effects of sodium hydrosulfide (NaHS), a H 2S donor, were evaluated on spontaneous contractile activity and after pre-contraction with bethanechol. l-Cysteine was evaluated as an endogenous H 2S donor. We evaluated extrinsic nerves, enteric nervous system, visceral afferent nerves, nitric oxide, K + ATP and K + CA channels, and myosin light chain phosphatase on action of H 2S using non-adrenergic/non-cholinergic conditions, tetrodotoxin, capsaicin, l-N G-nitro arginine (l-NNA), glibenclamide, apamin, and calyculin A, respectively, and electrical field stimulation (EFS). Results: NaHS dose-dependently and reversibly inhibited spontaneous and bethanechol-stimulated contractile activity (p < 0.05). l-Cysteine had a dose-dependent inhibitory effect. Non-adrenergic/non-cholinergic conditions, tetrodotoxin, capsaicin, l-NNA, or apamin had no effect on contractile inhibition by NaHS; in contrast, low-dose glibenclamide and calyculin A prevented NaHS-induced inhibition. We could not demonstrate H 2S release by EFS. Conclusions: H 2S inhibits contractile activity of jejunal circular muscle dose-dependently, in part by K + ATP channels and via myosin light chain phosphatase, but not via pathways mediated by the extrinsic or enteric nervous system, visceral afferent nerves, nitric oxide, or K + CA channels.
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