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Published ahead of print on August 20, 2007, doi:10.1165/rcmb.2007-0198TR
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American Journal of Respiratory Cell and Molecular Biology. Vol. 38, pp. 127-134, 2008
© 2008 American Thoracic Society
DOI: 10.1165/rcmb.2007-0198TR


Translational Review

Alveolar Epithelial β2-Adrenergic Receptors

Gökhan M. Mutlu1 and Phillip Factor2

1 Pulmonary and Critical Care Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois; and 2 Pulmonary, Allergy and Critical Care Medicine, Columbia University College of Physicians and Surgeons, New York, New York

Correspondence and requests for reprints should be addressed to Gökhan M. Mutlu, M.D., Northwestern University Feinberg School of Medicine, Pulmonary and Critical Care Medicine, 240 E. Huron Street, McGaw M-300, Chicago, IL 60611. Email: g-mutlu{at}northwestern.edu

β2-adrenergic receptors are present throughout the lung, including the alveolar airspace, where they play an important role for regulation of the active Na+ transport needed for clearance of excess fluid out of alveolar airspace. β2-adrenergic receptor signaling is required for up-regulation of alveolar epithelial active ion transport in the setting of excess alveolar edema. The positive, protective effects of β2-adrenergic receptor signaling on alveolar active Na+ transport in normal and injured lungs provide substantial support for the use of β-adrenergic agonists to accelerate alveolar fluid clearance in patients with cardiogenic and noncardiogenic pulmonary edema. In this review, we summarize the role of β2-adrenergic receptors in the alveolar epithelium with emphasis on their role in the regulation of alveolar active Na+ transport in normal and injured lungs.

Key Words: pulmonary edema • acute respiratory distress syndrome • acute lung injury • alveoli • albuterol


CLINICAL RELEVANCE

This review will help clinicians understand the mechanisms by which β2-adrenergic therapy may be useful in the management of acute lung injury.

 






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Copyright © 2008 American Thoracic Society.