4-Aminopyridine-sensitive K+ channels contributes to NaHS-induced membrane hyperpolarization and relaxation in the rat coronary artery

Wai San Cheang, Wing Tak Wong, Bing Shen, Chi Wai Lau, Xiao Yu Tian, Suk Ying Tsang, Xiaoqiang Yao, Zhen Yu Chen, Yu Huang

Research output: Contribution to journalArticlepeer-review

74 Scopus citations


The present study aimed at examining the role of potassium channels and endothelium in relaxations induced by sodium hydrogen sulphide (NaHS), which is the donor of gaseous hydrogen sulphide (H2S) and the effect of NaHS on endothelium-dependent relaxations in rat coronary arteries. Rat coronary arteries were suspended in a myograph for force measurement and changes of the membrane potential in arteries were determined by membrane potential-sensitive fluorescence dye. NaHS relaxed coronary arteries pre-contracted by U46619 and the relaxation was significantly less in high KCl-contracted rings. NaHS-induced relaxations were reduced by 4-aminopyridine (4-AP) but unaffected by glibenclamide, iberiotoxin, NG-nitro-L-arginine methyl ester, ODQ, indomethacin or by endothelium removal. The inhibitory effect of 4-AP was absent in NaHS-induced relaxations in high KCl-contracted rings. Addition of NaHS caused membrane hyperpolarization and this effect was inhibited by 4-AP but not by glibenclamide. NaHS causes endothelium-independent relaxations in rat coronary arteries partially through activation of 4-AP-sensitive potassium channel and ensuring hyperpolarization. Other potassium channels, Na+-K+ pump or endothelium-derived relaxing factors play little role.

Original languageEnglish (US)
Pages (from-to)94-98
Number of pages5
JournalVascular Pharmacology
Issue number3-4
StatePublished - Sep 2010


  • Coronary artery
  • Hydrogen sulphide
  • Potassium channel
  • Rat
  • Relaxation

ASJC Scopus subject areas

  • Physiology
  • Molecular Medicine
  • Pharmacology


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