Redox signaling in oxygen sensing by vessels

E. Kenneth Weir, Zhigang Hong, Valerie A. Porter, Helen L. Reeve

Research output: Contribution to journalArticlepeer-review

46 Scopus citations

Abstract

In response to the increase in oxygen tension at birth, the resistance pulmonary arteries dilate, while the ductus arteriosus constricts. Although modulated by the endothelium, these opposite responses are intrinsic to the vascular smooth muscle. While still controversial, it seems likely that during normoxia the production of reactive oxygen species (ROS) increases and the smooth muscle cell cytoplasm is more oxidized in both pulmonary arteries and ductus, compared to hypoxia. However, the effect of changes in the endogenous redox status or the addition of a redox agent, oxidizing or reducing, is exactly opposite in the two vessels. A reducing agent, dithiothreitol, like hypoxia, in the pulmonary artery will inhibit potassium current, cause depolarization, increase cytosolic calcium and lead to contraction. Responses to dithiothreitol in the ductus are opposite and removal of endogenous H2O2 by intracellular catalase in the ductus increases potassium current. Oxygen sensing in both vessels is probably mediated by redox effects on both calcium influx and calcium release from the sarcoplasmic reticulum (SR).

Original languageEnglish (US)
Pages (from-to)121-130
Number of pages10
JournalRespiratory Physiology and Neurobiology
Volume132
Issue number1
DOIs
StatePublished - Aug 22 2002

Keywords

  • Endothelium, pulmonary
  • Oxygen, sensing in pulmonary vessels
  • Pulmonary vasculature, oxygen sensing
  • Redox state, pulmonary vessels
  • Smooth muscle, pulmonary vessels

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