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Dopamine Regulates NA,K-Adenosine Triphosphatase in Alveolar Epithelial Cells via the Mitogen-Activated Protein Kinase/Extracellular-Signal-Regulated Kinase Pathway*

C. Guerrero; A. Ghosh; E. Lecuona; K. Ridge; E. Santos; J.I. Sznajder, MD, FCCP
Author and Funding Information

*From the Division of Pulmonary and Critical Care Medicine, Michael Reese Hospital, University of Illinois at Chicago, Chicago, IL, and National Cancer Institute, National Institutes of Health, Bethesda, MD.

Correspondence to: J.I. Sznajder MD, FCCP, Department of Medicine, Michael Reese Hospital and Medical Center, 2929 S Ellis Ave, Baum-101, Chicago, IL 60616



Chest. 1999;116(suppl_1):88S-89S. doi:10.1378/chest.116.suppl_1.88S
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Extract

Alveolar epithelial Na,K-adenosine triphosphatase (ATPase) plays an important role in lung edema clearance.1 Na,K-ATPase is an integral membrane protein consisting of the α subunit, which has catalytic activity and ion binding sites,2 and the β subunit, which plays a regulatory role contributing to the stability of the complex and its insertion in the plasma membrane.3 Dopamine (DA) upregulates the Na,K-ATPase in the alveolar epithelium and increases lung liquid clearance,4 but the mechanisms of this regulation have not been elucidated. The mitogen-activated protein kinase (MAPK), also known as extracellular-signal-regulated kinase (ERK) cascade, is a major signaling system by which cells transduce extracellular signals into intracellular responses.5 In mammalian cells ERK proteins, ERK1 and ERK2, also known as p44/p42 respectively, are activated by a variety of hormones, growth factors, and peptides.6 Little is known about ERK activation by catecholamines and we are not aware of studies about ERK activation in alveolar type II (ATII) cells. Thus, we tested whether ERK proteins are activated by DA in ATII cells and whether this activation is involved in the upregulation of the Na,K-ATPase in these cells.


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