Nitric oxide modulates a calcium-activated potassium current in muscle cells from opossum esophagus

J. A. Murray, E. F. Shibata, T. L. Buresh, H. Picken, B. W. O'Meara, J. L. Conklin

Research output: Contribution to journalArticlepeer-review

38 Scopus citations


Nitric oxide mediates nerve-induced hyperpolarization of circular smooth muscle of the esophagus. Two mechanisms are proposed to explain this hyperpolarization: an increase in K+ current or a decrease in Cl current. These studies test the hypothesis that nitric oxide increases a K+ current in esophageal smooth muscle. Three outward K+ currents are present in circular smooth muscle cells from the opossum esophagus. One current is a Ca2+-activated K+ current (I(KCa2+)). This current is inhibited by charybdotoxin. Whole cell currents were recorded from isolated opossum esophageal smooth muscle cells using the whole cell patch-clamp technique. These studies showed that I(KCa2+) is activated at potentials more positive than -30 mV. Bath application of S-nitroso-L-cysteine increased I(KCa2+) by 50% above control levels throughout the entire activation range of potentials. The enhanced current was reversible on washout. Either charybdotoxin, an inhibitor of I(KCa2+), or (R)-p-8-(4-chlorophenylthio)- guanosine 3',5'-cyclic monophosphorothioate, an inhibitor of protein kinase G, antagonized the increase in outward current induced by S-nitroso-L- cysteine. These data suggest that nitric oxide activates I(KCa2+) via the guanosine 3',5'-cyclic monophosphate-protein kinase G signal transduction pathway.

Original languageEnglish (US)
Pages (from-to)G606-G612
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Issue number4 32-4
StatePublished - 1995


  • charybdotoxin
  • cyclic guanidino-monophosphate
  • esophageal motility
  • guanyl cyclase
  • hyperpolarization
  • patch clamp
  • potassium currents
  • smooth muscle

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)


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