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Am J Physiol Lung Cell Mol Physiol (May 16, 2003). doi:10.1152/ajplung.00339.2002
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Submitted on October 10, 2002
Accepted on May 14, 2003

Post-receptor defects in alveolar epithelial {beta}-adrenergic signaling after prolonged isoproterenol infusion

Eric E. Morgan1, Sonya M. Stader1, Cheryl M. Hodnichak1, Kate E. Mavrich1, Hans G. Folkesson1, and Michael B. Maron1*

1 Department of Physiology, Northeastern Ohio Universities College of Medicine, Rootstown, OH, USA

* To whom correspondence should be addressed. E-mail: mbm{at}neoucom.edu.

We previously found that prolonged isoproterenol (Iso) infusion in rats impaired the ability of {beta}-adrenoceptor ({beta}AR) agonists to increase alveolar liquid clearance (ALC). Here, we determined if post-receptor defects in {beta}AR signaling contribute to this impairment. Iso was infused using subcutaneous miniosmotic pumps (4, 40, or 400 µg/kg/h) in rats for 48 hr. At this time, forskolin-stimulated ALC was measured by mass-balance. Forskolin-stimulated ALC (33.4±2.1 (SE) %/h in vehicle-infused rats) was reduced by 25 and 38%, respectively, after the 40 and 400 µg/kg/h Iso infusions. The ability of forskolin to increase cAMP was reduced by 70% in ATII cells isolated from rats infused with Iso at 400 µg/kg/h. Additionally, the ability of the stable cAMP analog Sp-8-Bromo-cAMPS to increase ALC (48.7±3.0% in vehicle-infused rats) was reduced by 25 and 51%, respectively, after the 40 and 400 µg/kg/h infusions. Finally, the ability of cAMP to increase PKA activity was eliminated in ATII cells isolated from rats infused with Iso at 400 µg/kg/h. These data demonstrate that prolonged {beta}AR-agonist exposure can impair alveolar epithelial {beta}AR signaling downstream of the {beta}AR.




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