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Articles in PresS, published online ahead of print December 14, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00381.2001
Submitted on September 25, 2001
Accepted on December 6, 2001
1 Physiology, Northeastern Ohio Universities College of Medicine, Rootstown, OH, USA
* To whom correspondence should be addressed. E-mail: mbm{at}neoucom.edu.
We determined if prolonged isoproterenol (iso) infusion in rats impaired the ability of the ß2-adrenergic agonist terbutaline to increase alveolar liquid clearance (ALC). Rats were infused with iso (at rates of 4, 40, or 400 µg/kg/h) or vehicle (0.001 N HCl) for 48 hr using subcutaneously implanted miniosmotic pumps. After this time, the rats were anesthetized, and ALC was determined (by mass-balance after instillation of Ringers lactate containing albumin into the lungs) under baseline conditions and after terbutaline administration. Baseline and terbutaline-stimulated ALC in vehicle-infused rats averaged, respectively, 19.6±1.2% (SE) and 44.7±1.5%/h. The ability of terbutaline to increase ALC was eliminated at 400 µg/kg/h iso, inhibited by 26% at 40 µg/kg/h iso, and was minimally affected by 4 µg/kg/h iso. ß-adrenergic receptor (ßAR) density of freshly isolated alveolar epithelial type II (ATII) cells from iso-infused rats was reduced by the 40 and 400 µg/kg/h infusion rates. These data demonstrate that prolonged exposure to ß-agonists can impair the ability of ß2-agonists to stimulate ALC and produce ATII cell ßAR downregulation.
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