O2 sensing in hypoxic pulmonary vasoconstriction: The mitochondrial door re-opens

Gregory B. Waypa, Paul T. Schumacker*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

55 Scopus citations

Abstract

The identity of the O2 sensor underlying the hypoxic pulmonary vasoconstriction (HPV) response has been sought for more than 50 years. Recently, the mitochondria have again come into sharp focus as the cellular organelle responsible for triggering the events that culminate in pulmonary artery constriction. Studies from different laboratories propose two disparate models to explain how mitochondria react to a decrease in PO2. One model proposes that hypoxia slows or inhibits mitochondrial electron transport resulting in the accumulation of reducing equivalents and a decrease in the generation of reactive oxygen species (ROS). This is proposed to activate a redox-sensitive pathway leading to pulmonary vasoconstriction. A second and opposing model suggests that hypoxia triggers a paradoxical increase in mitochondrial ROS generation. This increase would then lead to the activation of an oxidant-sensitive signaling transduction pathway leading to HPV. This article summarizes the potential involvement of mitochondria in these two very different models.

Original languageEnglish (US)
Pages (from-to)81-91
Number of pages11
JournalRespiratory Physiology and Neurobiology
Volume132
Issue number1
DOIs
StatePublished - Aug 22 2002

Keywords

  • Blood, flow, pulmonary
  • Hypoxia, pulmonary vasoconstriction
  • Mitochondria, reactive oxygen species
  • Oxygen, reactive species, HPV
  • Perfusion, pulmonary

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology
  • Pulmonary and Respiratory Medicine

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