Hydrogen trisulfide induced modulation of vascular tone in mice aorta

[Speaker] Shigeto Suzuki:1
[Co-author] Shigeki Kiuchi:1, Hideo Kimura:2, Kageyoshi Ono:1
1:Laboratory of Molecular Physiology and Pharmacology, Faculty of Pharma-Science, Teikyo University, Japan, 2:Department of Molecular Pharmacology, National Center of Neurology and Psychiatry, National Institute of Neuroscience, Japan

Background: Hydrogen sulfide (H2S) is produced in various tissues and organs such as brain, pancreas, heart and blood vessels, playing important roles in neurotransmission, insulin secretion, cardioprotection and regulation of vascular tone. A number of reports have shown that H2S induces contraction and/or relaxation in blood vessels depending on its condition. Recent works revealed hydrogen trisulfide (H2S3) is also a potential signal modulating molecule. The present study was aimed at elucidating the effects of H2S3 on vascular tone and their mechanisms.
Methods: Ring segments were prepared from mice thoracic aorta and changes in vascular tension were recorded isometrically with force displacement transducers. Sodium trisulfide (Na2S3) was used as a H2S3 donor. Na2S3 (10 - 100 μM) was applied to phenylephrine (1 μM)-precontracted mice aortic rings. Experiments were performed with endothelium intact and endothelium removed preparations.
Results: Na2S3 evoked transient contraction, followed by sustained relaxation, in the phenylephrine-precontracted aorta. The Na2S3-induced contraction was eliminated by endothelium denudation or pretreatment with NG-nitro-L-arginine (L-NNA). The Na2S3-induced relaxation was also diminished in the presence of L-NNA or endothelium removal, but it was not completely eliminated. This L-NNA insensitive and endothelium-independent fraction of Na2S3-induced vasodilatation was further suppressed by a NO scavenger carboxy-PTIO, or 4-aminopyridine, but not by glibenclamide.
Conclusion: Present results indicate that H2S3 evokes apparent vasoconstrction by inhibiting NO production in endothelium and that H2S3 induces vasorelaxation by directly acting on vascular smooth muscle through a NO-dependent mechanism and/or activation of Kv channels.

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