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Published ahead of print on July 15, 2004, doi:10.1164/rccm.200308-1127OC

Am. J. Respir. Crit. Care Med., Volume 170, Number 7, October 2004, 730-736

A more recent version of this article appeared on October 1, 2004
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Submitted on September 11, 2003
Accepted on July 9, 2004

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

Zaher S Azzam1, Yochai Adir1, Astrid Crespo2, Alejandro Comellas3, Emilia Lecuona3, Laura A Dada3, Norberto Krivoy3, David H Rutschman4, Jacob I Sznajder3, and Karen M Ridge5*

1 Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, IL, USA; Technion, Israel Institute of Technology, Haifa, Israel, 2 Universidad Central de Venezuela, Caracas, Venezuela, 3 Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, IL, USA, 4 Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, IL, USA; Northeastern Illinois University, Chicago, IL, USA, 5 Medical Service, Veteran Affairs Chicago Health Care System, Chicago, IL, USA; Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, IL, USA

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

The purpose of this study was to determine whether {alpha}-adrenergic receptor agonists have a role in alveolar fluid reabsorption, via Na,K-ATPase, in the alveolar epithelium. Alveolar fluid reabsorption increased ~ 2-fold with increasing concentrations of NE as compared to control rats. Treatment with the non-selective {alpha}-adrenergic receptor agonist, octopamine and the specific {alpha}1 agonist, phenylephrine, increased alveolar fluid reabsorption by 54% and 40% respectively as compared to control. The specific {alpha}1-adrenergic receptor antagonist, prazosin, inhibited the stimulatory effects of NE by ~30%, whereas {alpha}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 {alpha}1-and {beta}-adrenergic receptor. In conclusion, we report here, that NE increased alveolar fluid reabsorption via the activation of both {alpha}1 and {beta}-adrenergic receptors, but not {alpha}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: Na,K-ATPase, norepinephrine, alveolar fluid reabsorption




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