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Norepinephrine Increases Alveolar Fluid Reabsorption and Na,K-ATPase Activity

Medical Service, Veteran Affairs Chicago Health Care System; Division of Pulmonary and Critical Care Medicine, Northwestern University; and Northeastern Illinois University, Chicago, Illinois; Technion, Israel Institute of Technology, Haifa, Israel; and Universidad Central de Venezuela, Caracas, Venezuela

Correspondence and requests for reprints should be addressed to Karen M. Ridge, Ph.D., Pulmonary and Critical Care Medicine, Northwestern University, Tarry 14-707, 300 E. Superior Street, Chicago, IL 60616. E-mail: kridge{at}northwestern.edu

The purpose of this study was to determine whether -adrenergic receptor agonists have a role in alveolar fluid reabsorption, via Na,K-ATPase, in the alveolar epithelium. Alveolar fluid reabsorption increased approximately twofold with increasing concentrations of norepinephrine (NE) as compared with control rats. Treatment with the nonselective -adrenergic receptor agonist, octopamine, and the specific ₁ agonist, phenylephrine, increased alveolar fluid reabsorption by 54 and 40%, respectively, as compared with control. The specific ₁-adrenergic receptor antagonist, prazosin, inhibited the stimulatory effects of NE by approximately 30%, whereas ₂-adrenergic antagonist, yohimbine, did not prevent the stimulatory effects of NE. The administration of ouabain, Na,K-ATPase inhibitor, prevented the NE-mediated increase in alveolar fluid reabsorption. In parallel with these changes, NE increased Na,K-ATPase activity and protein abundance in alveolar epithelial type II cells via the ₁- and ß-adrenergic receptor. We report here that NE increased alveolar fluid reabsorption via the activation of both ₁- and ß-adrenergic receptors, but not ₂-adrenergic receptors. These effects are due to increased activity and abundance of the Na,K-ATPase in the basolateral membrane of ATII cells.

Key Words: -adrenergic receptors • active Na⁺ transport • alveolar fluid reabsorption • Na,K-ATPase • norepinephrine

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