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Articles in PresS, published online ahead of print August 6, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00085.2002
Submitted on March 4, 2002
Accepted on July 23, 2002
1 Department of Internal Medicine and Section of Nephrology, Yale University School of Medicine, New Haven, CT, USA
* To whom correspondence should be addressed. E-mail: John.Hayslett{at}yale.edu.
There are conflicting reports in the literature regarding the adenosine receptor that mediates the increase in sodium transport in the A6 cell. In this study we used specific A1 and A2 adenosine receptor agonists and antagonists, as well as two different subclones of the A6 cell, to determine which adenosine receptor mediates the increase in sodium transport. In the A6S2 subclone, basolateral and apical CHA, a selective A1 receptor agonist, stimulated sodium transport at a threshold concentration less than 10-7M, whereas CGS 21680, a selective A2 receptor agonist, had a threshold concentration that was at least 10-5M. The A1 receptor antagonist DPCPX was found to have a nonspecific effect on CHA-stimulated sodium transport, whereas the A2 receptor antagonist CSC had no effect. As with the A6S2 subclone, basolateral and apical CHA stimulated sodium transport at a nanomolar concentration in the A6C1 subclone and the threshold concentration for CGS 21680 was in the high micromolar range. Concurrent with the increase in sodium transport, CHA also stimulated anion secretion in the A6C1 subclone. These data demonstrate that adenosine increases sodium transport via the A1 receptor in different subclones of the A6 cell, including a subclone capable of anion secretion.
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