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2-adrenergic receptor stimulation on alveolar fluid
clearance in mice
1 Cardiovascular Research Institute, University of California, San Francisco, California 94143-0130; 2 Botnar Center of Clinical Research, CHUV, Lausanne, 1011 Switzerland; 3 Department of Medicine, University of Cincinnati, Cincinnati, Ohio 45267-0564; 4 Sepracor, Marlborough, Massachusetts 01752; and 5 Department of Physiology, Northeastern Ohio University College of Medicine, Rootstown, Ohio 44272-0095
Stimulation of active fluid transport
with 
-adrenergic receptor (AR) agonists can accelerate the
resolution of alveolar edema. However, chronic AR-agonist
administration may cause AR desensitization and downregulation that
may impair physiological responsiveness to AR-agonist stimulation.
Therefore, we measured baseline and terbutaline- (10
3 M)
stimulated alveolar fluid clearance in mice that received subcutaneously (miniosmotic pumps) either saline or albuterol (2 mg · kg1 · day1)
for 1, 3, or 6 days. Continuous albuterol administration increased plasma albuterol levels (105 M), an effect that was
associated with 1) a significant decrease in AR density
and 2) attenuation, but not ablation, of maximal terbutaline-induced cAMP production. Forskolin-mediated cAMP-release was unaffected. Continuous albuterol infusion stimulated alveolar fluid
clearance on day 1 but did not increase alveolar fluid
clearance on days 3 and 6. However,
terbutaline-stimulated alveolar fluid clearance in albuterol-treated
mice was not reduced compared with saline-treated mice. Despite
significant reductions in AR density and agonist-mediated cAMP
production by long-term AR-agonist exposure, maximal
AR-agonist-mediated increase in alveolar fluid clearance is not
diminished in mice.
pulmonary edema; acute lung injury; lung fluid balance; alveolar epithelium
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