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Postreceptor defects in alveolar epithelial -adrenergic signaling after prolonged isoproterenol infusion

Department of Physiology, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio 44272-0095

Submitted 10 October 2002 ; accepted in final form 14 May 2003

We previously found that prolonged isoproterenol (Iso) infusion in rats impaired the ability of -adrenoceptor (-AR) agonists to increase alveolar liquid clearance (ALC). Here, we determined if postreceptor defects in -AR signaling contribute to this impairment. Iso was infused using subcutaneous miniosmotic pumps (4, 40, or 400 µg · kg^-1 · h^-1) in rats for 48 h. At this time, forskolin-stimulated ALC was measured by mass balance. Forskolin-stimulated ALC [33.4 ± 2.1%/h (mean ± SE) in vehicle-infused rats] was reduced by 25 and 38%, respectively, after the 40 and 400 µg · kg^-1 · h^-1 Iso infusions. The ability of forskolin to increase cAMP was reduced by 70% in alveolar type II (ATII) cells isolated from rats infused with 400 µg · kg^-1 · h^-1 Iso. Additionally, the ability of the stable cAMP analog 8-bromoadenosine-3',5'-cyclic monophosphorothioate, Sp-isomer, 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^-1 · h^-1 infusions. Finally, the ability of cAMP to increase protein kinase A activity was eliminated in ATII cells isolated from rats infused with Iso at 400 µg · kg^-1 · h^-1. These data demonstrate that prolonged -AR agonist exposure can impair alveolar epithelial -AR signaling downstream of the -AR.

pulmonary edema; -adrenergic receptor signaling pathway; receptor desensitization; alveolar epithelial type II cells; adenylyl cyclase; adenosine 3',5'-cyclic monophosphate; protein kinase A

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