Mechanisms of Action of the Gasotransmitter Hydrogen Sulfide in Modulating Contractile Activity of Longitudinal Muscle of Rat Ileum

Munenori Nagao, David R Linden, Judith A. Duenes, Michael G. Sarr

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Aim: This study aims to determine mechanisms of action of the gasotransmitter hydrogen sulfide (H2S) 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 H2S, were evaluated on spontaneous contractile activity and after enhanced contractile activity with bethanechol. l-cysteine was evaluated as a potential endogenous donor of H2S. We evaluated involvement of extrinsic nerves, enteric nervous system, visceral afferent nerves, nitric oxide, and KATP+ channel and KCa+ channel activity on the action of H2S using non-adrenergic/non-cholinergic conditions, tetrodotoxin, capsaicin, l-NG-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 H2S release by electrical field stimulation but did show that inhibition of cystathionine β synthase, an endogenous source of H2S, augmented the inhibitory effect of low-frequency electrical field stimulation. Conclusion: H2S 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, KATP+ channels, or KCa+ channels.

Original languageEnglish (US)
Pages (from-to)12-22
Number of pages11
JournalJournal of Gastrointestinal Surgery
Volume15
Issue number1
DOIs
StatePublished - 2011

Fingerprint

Gasotransmitters
Hydrogen Sulfide
Bethanechol
Apamin
Ileum
Tetrodotoxin
Visceral Afferents
Electric Stimulation
Enteric Nervous System
Muscles
KATP Channels
Glyburide
Capsaicin
Cysteine
Arginine
Nitric Oxide
Cystathionine
Isometric Contraction
sodium bisulfide

Keywords

  • Contractile activity
  • Gasotransmitter
  • Hydrogen sulfide
  • Ileum longitudinal smooth muscle
  • Intestinal motility
  • Longitudinal muscle
  • Motility
  • Physiology

ASJC Scopus subject areas

  • Surgery
  • Gastroenterology

Cite this

Mechanisms of Action of the Gasotransmitter Hydrogen Sulfide in Modulating Contractile Activity of Longitudinal Muscle of Rat Ileum. / Nagao, Munenori; Linden, David R; Duenes, Judith A.; Sarr, Michael G.

In: Journal of Gastrointestinal Surgery, Vol. 15, No. 1, 2011, p. 12-22.

Research output: Contribution to journalArticle

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abstract = "Aim: This study aims to determine mechanisms of action of the gasotransmitter hydrogen sulfide (H2S) 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 H2S, were evaluated on spontaneous contractile activity and after enhanced contractile activity with bethanechol. l-cysteine was evaluated as a potential endogenous donor of H2S. We evaluated involvement of extrinsic nerves, enteric nervous system, visceral afferent nerves, nitric oxide, and KATP+ channel and KCa+ channel activity on the action of H2S using non-adrenergic/non-cholinergic conditions, tetrodotoxin, capsaicin, l-NG-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 H2S release by electrical field stimulation but did show that inhibition of cystathionine β synthase, an endogenous source of H2S, augmented the inhibitory effect of low-frequency electrical field stimulation. Conclusion: H2S 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, KATP+ channels, or KCa+ channels.",
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AB - Aim: This study aims to determine mechanisms of action of the gasotransmitter hydrogen sulfide (H2S) 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 H2S, were evaluated on spontaneous contractile activity and after enhanced contractile activity with bethanechol. l-cysteine was evaluated as a potential endogenous donor of H2S. We evaluated involvement of extrinsic nerves, enteric nervous system, visceral afferent nerves, nitric oxide, and KATP+ channel and KCa+ channel activity on the action of H2S using non-adrenergic/non-cholinergic conditions, tetrodotoxin, capsaicin, l-NG-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 H2S release by electrical field stimulation but did show that inhibition of cystathionine β synthase, an endogenous source of H2S, augmented the inhibitory effect of low-frequency electrical field stimulation. Conclusion: H2S 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, KATP+ channels, or KCa+ channels.

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