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Published ahead of print on March 23, 2004, doi:10.1165/rcmb.2004-0012OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 2, August 2004, 140-146

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Submitted on January 13, 2004
Revised on March 17, 2004

Activation of airway Cl- secretion in human subjects by adenosine

Karen Hentchel-Franks1, David Lozano1, Valerie L Eubanks-Tarn1, Bryan R Cobb2, Lijuan Fan1, Robert Oster3, Eric J Sorscher4, and John P Clancy1*

1 Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, USA; Gregory Fleming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, AL, USA, 2 Department of Human Genetics, Georgetown University, Washington, DC, USA, 3 Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA, 4 Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA; Gregory Fleming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, AL, USA

* To whom correspondence should be addressed. E-mail: jclancy{at}peds.uab.edu.

We investigated CFTR regulation by A2 adenosine receptors and {beta}2 adrenergic receptors in CFTR-corrected CFBE41o- airway cells and human subjects. CFBE41o- cells stimulated with adenosine (Ado, 10 µM), isoproterenol (Iso, 10 µM), or Ado + Iso (10 µM each) elevated cAMP above control conditions (p<0.001), with the Iso conditions increasing cAMP approximately 10-fold above that produced by Ado alone (p<0.001). All agonist conditions had similar effects on Isc at 10 and 25 µM, with no further currents produced by subsequent stimulation with forskolin (20 µM). CFTR-dependence was demonstrated by glybenclamide block of agonist stimulated currents. Nasal potential difference studies in normal (n=50) subjects demonstrated that Ado (10 µM) and Ado + Iso (10 µM each) produced more polarization compared with Iso (10 µM Ado increase = 44%, 10 µM Ado + Iso increase = 52%, p<0.05 for each condition compared with Iso alone). Studies completed in CF patients (n=10, "severe" genotypes) confirmed that Ado-stimulated polarization was CFTR dependent. Together, these results indicate that Ado is a potent Cl- secretagogue in vivo, with relatively small effects on cAMP levels despite strong effects on CFTR dependent Isc and nasal Cl- transport. These findings support growing evidence indicating a role for Ado regulation of CFTR-dependent Cl-secretion in vivo.




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