title: Generation of oxidants by hypoxic human pulmonary and coronary smooth-muscle cells.
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.
authors.affiliation: Department of Medicine, Division of Pulmonary, Critical Care and Sleep Disorders, University of Louisville and Louisville Veterans' Administration Medical Center, Louisville, KY. Electronic address: jinesh.mehta@louisville.edu.
authors.forename: Jinesh P
authors.initials: JP
authors.lastname: Mehta
authors.affiliation: Molecular Targets Program, J.G. Brown Cancer Center, University of Louisville, Louisville, KY.
authors.forename: Jian Li
authors.initials: JL
authors.lastname: Campian
authors.affiliation: Department of Medicine, Division of Pulmonary, Critical Care and Sleep Disorders, University of Louisville and Louisville Veterans' Administration Medical Center, Louisville, KY.
authors.forename: Juan
authors.initials: J
authors.lastname: Guardiola
authors.affiliation: Minneapolis Veterans' Administration Medical Center, Department of Surgery, Division of Cardiothoracic Surgery, University of Minnesota, Minneapolis, MN.
authors.forename: Jesus A
authors.initials: JA
authors.lastname: Cabrera
authors.affiliation: Department of Medicine, Division of Cardiology, University of Minnesota, Minneapolis, MN.
authors.forename: E Kenneth
authors.initials: EK
authors.lastname: Weir
authors.affiliation: Molecular Targets Program, J.G. Brown Cancer Center, University of Louisville, Louisville, KY.
authors.forename: John W
authors.initials: JW
authors.lastname: Eaton
mesh_terms: D002478:Cells, Cultured; D003331:Coronary Vessels; D006801:Humans; D000860:Hypoxia / Q000378:metabolism*; D066298:In Vitro Techniques; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D011651:Pulmonary Artery; D017382:Reactive Oxygen Species / Q000378:metabolism*; D014661:Vasoconstriction
chemical_list: D017382:Reactive Oxygen Species