Generation of oxidants by hypoxic human pulmonary and coronary smooth-muscle cells

Jinesh P. Mehta, Jian Li Campian, Juan Guardiola, Jesus A. Cabrera, E. Kenneth Weir, John W. Eaton

Research output: Contribution to journalArticlepeer-review

24 Scopus citations

Abstract

Background: Pulmonary vasoconstriction in response to hypoxia is unusual inasmuch as local exposure of nonpulmonary vasculature to hypoxia results in vasodilation. It has been suggested that pulmonary artery smooth-muscle cells may relax in response to intracellular generation of reactive oxygen species (ROS) and that the production of ROS decreases under hypoxia. However, other workers report increased ROS production in human pulmonary artery smooth-muscle cells (HPASMC) during hypoxia. Methods: Using dihydrodichlorofluorescein diacetate, dihydroethidium, and Amplex Red (Molecular Probes; Eugene, OR), we estimated ROS generation by confluent primary cultures of HPASMC and human coronary artery smooth-muscle cells (HCASMC) under normoxia (20%) and acute hypoxia (5%). Results: All three assay systems showed that HPASMC production of ROS is decreased under hypoxia and to a greater extent than the decrease in ROS production by HCASMC. A substantially greater percentage of normoxic ROS production by HPASMC is mitochondrial (> 60%) compared to HCASMC (< 30%). Conclusions: These results support the conclusion that ROS generation decreases, rather than increases, in HPASMC during hypoxia. However, as ROS production also decreases in HCASMC during hypoxia, the reason for the opposite change in vascular tone is not yet apparent.

Original languageEnglish (US)
Pages (from-to)1410-1414
Number of pages5
JournalCHEST
Volume133
Issue number6
DOIs
StatePublished - Jun 2008

Keywords

  • Coronary
  • Human
  • Hypoxia
  • Pulmonary
  • Reactive oxygen species
  • Smooth-muscle cells

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