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Generation of Oxidants by Hypoxic Human Pulmonary and Coronary Smooth Muscle Cells

¹Department of Medicine, Division of Pulmonary, Critical Care and Sleep Disorders, University of Louisville and Louisville Veterans' Administration Medical Center ²Molecular Targets Program, J.G. Brown Cancer Center, University of Louisville ³Minneapolis Veterans' Administration Medical Center, Department of Surgery, Division of Cardiothoracic Surgery, University of Minnesota ⁴Minneapolis Veterans' Administration Medical Center, Department of Medicine, Division of Cardiology, University of Minnesota

jinesh.mehta{at}louisville.edu

Abstract

Background: Pulmonary vasoconstriction in response to hypoxia is unusual inasmuch as local exposure of non-pulmonary vasculature to hypoxia results in vasodilation. It has been suggested that pulmonary artery smooth muscle (PASMC) 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 HPASMCs during hypoxia.

Methods: Using dihydrodichlorofluorescein diacetate, dihydroethidium and Amplex^® Red we estimated ROS generation by confluent primary cultures of human PASMC (HPASMC) and human coronary artery smooth 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 HPASMCs during hypoxia. However, as ROS production also decreases in HCASMCs during hypoxia, the reason for the opposite change in vascular tone is not yet apparent.

Key Words: Hypoxia • Reactive oxygen species (ROS) • Pulmonary • Coronary • Smooth muscle cells • Human