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Articles in PresS, published online ahead of print August 2, 2002
J Appl Physiol, 10.1152/jap.00275.2002
Submitted on March 29, 2002
Accepted on July 18, 2002
1 Cardiovascular Research Institute, University of California, San Francisco, CA, USA; Botnar Center of Clinical Research, CHUV, Laussanne, Switzerland
2 Cardiovascular Research Institute, University of California, San Francisco, CA, USA
3 Department of Medicine, University of Cincinnati, Cincinnati, OH, USA
4 Sepracor, Inc., Marborough, MA, USA
5 Department of Physiology, Northeastern Ohio University College of Medicine, Rootstown, OH, USA
* To whom correspondence should be addressed. E-mail: hgfolkes{at}neoucom.edu.
Stimulation of active fluid transport with ß-adrenergic receptor (ßAR) agonists can accelerate the resolution of alveolar edema. However, chronic ßAR-agonist administration may cause ßAR-desensitization and -downregulation that may impair physiological responsiveness to ßAR-agonist stimulation. Therefore, we measured baseline and terbutaline (10-3 M) stimulated alveolar fluid clearance in mice that received subcutaneously (mini-osmotic pumps) either saline or albuterol (2 mg/kg/day) for 1, 3, or 6 days. Continuous albuterol administration increased plasma albuterol levels (10-5 M), an effect that was associated with (1) a significant decrease in ßAR density, and (2) attenuation, but not ablation, of maximal terbutaline-induced cAMP production. Forskolin-mediated cAMP-release was unaffected. Continuous albuterol-infusion stimulated alveolar fluid clearance on day 1, but did not increase alveolar fluid clearance on day 3 and 6. However, terbutaline-stimulated alveolar fluid clearance in albuterol-treated mice was not reduced compared to saline-treated mice. Despite significant reductions in ßAR density and agonist mediated cAMP production by long-term ßAR-agonist exposure, maximal ßAR-agonist-mediated increase in alveolar fluid clearance is not diminished in mice.
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