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Am J Physiol Lung Cell Mol Physiol 281: L895-L903, 2001;
1040-0605/01 $5.00
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Vol. 281, Issue 4, L895-L903, October 2001

Targeted transgenic expression of beta 2-adrenergic receptors to type II cells increases alveolar fluid clearance

Dennis W. McGraw1,*, Norimasa Fukuda2,*, Paul F. James3,*, Susan L. Forbes1, Alison L. Woo4, Jerry B. Lingrel4, David P. Witte5, Michael A. Matthay2, and Stephen B. Liggett1,3

Departments of 1 Medicine and 4 Molecular Genetics, University of Cincinnati College of Medicine, Cincinnati 45267, 3 Department of Zoology, Miami University, Oxford 45056; 5 Department of Pathology, Children's Hospital Medical Center, Cincinnati, Ohio 45229; and 2 Cardiovascular Research Institute, University of California, San Francisco, California 94143

Clearance of edema fluid from the alveolar space can be enhanced by endogenous and exogenous beta -agonists. To selectively delineate the effects of alveolar type II (ATII) cell beta 2-adrenergic receptors (beta 2-ARs) on alveolar fluid clearance (AFC), we generated transgenic (TG) mice that overexpressed the human beta 2-AR under control of the rat surfactant protein C promoter. In situ hybridization showed that transgene expression was consistent with the distribution of ATII cells. TG mice expressed 4.8-fold greater beta 2-ARs than nontransgenic (NTG) mice (939 ± 113 vs. 194 ± 18 fmol/mg protein; P < 0.001). Basal AFC in TG mice was ~40% greater than that in untreated NTG mice (15 ± 1.4 vs. 10.9 ± 0.6%; P < 0.005) and approached that of NTG mice treated with the beta -agonist formoterol (19.8 ± 2.2%; P = not significant). Adrenalectomy decreased basal AFC in TG mice to 9.7 ± 0.5% but had no effect on NTG mice (11.5 ± 1.0%). Na+-K+-ATPase alpha 1-isoform expression was unchanged, whereas alpha 2-isoform expression was ~80% greater in the TG mice. These findings show that beta 2-AR overexpression can be an effective means to increase AFC in the absence of exogenous agonists and that AFC can be stimulated by activation of beta 2-ARs specifically expressed on ATII cells.

G protein; adenylyl cyclase; beta -agonist; mouse; pulmonary edema

* Dennis W. McGraw, Norimasa Fukuda, and Paul F. James contributed equally to this work.




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