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Am J Physiol Renal Physiol (March 13, 2007). doi:10.1152/ajprenal.00382.2006
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Submitted on September 26, 2006
Accepted on March 9, 2007

Basolateral P2X4-like receptors regulate the extracellular ATP-stimulated epithelial Na+ channel activity in renal epithelia

Yanjun Zhang1, Daniel Sanchez1, Julia Gorelik2, David Klenerman3, Max Lab4, Christopher Edwards5, and Yuri Korchev1*

1 medicine, imperial college london, london, London, United Kingdom
2 National Heart and Lung Institute, Imperial College London, london, London, United Kingdom
3 Chemistry, cambridge university, cambrige, Cambridge, United Kingdom
4 london, London, United Kingdom; medicine, imperial college london, london, London, United Kingdom
5 University of Newcastle upon Tyne, Newcastle upon Tyne , United Kingdom

* To whom correspondence should be addressed. E-mail: y.korchev{at}imperial.ac.uk.

Extracellular ATP initiates potent effects on sodium transport across renal epithelia through membrane-associated purinergic receptors. Dependent on the location of these receptors ATP either inhibits or stimulates sodium reabsorption. Using A6 cells, transepithelial electrical resistance measurements and scanning ion conductance microscopy, we have identified the purinergic receptors involved in the stimulatory action on the epithelial cell basolateral plasma membrane. Addition of the potent P2X4 receptor agonist, 2MeSATP, to the basolateral side of the A6 monolayer stimulated amiloride-sensitive sodium conductance and produced similar cell morphological changes to those found with ATP{gamma}S, aldosterone or hypotonic stress. The agonist potency order determined by sodium conductance changes of the monolayer was: 2MeSATP ≥ ATP{gamma}S > CTP, a similar agonist potency profile to that of cloned P2X4 receptors but with higher sensitivity for {beta}{gamma}meATP and {alpha}{beta}meATP. We further demonstrated that the ATP effect on sodium transport was: potentiated by ivermectin; not blocked by suramin and PPADS; enhanced by Zn2+ but not by Cu2+; and significantly reduced but not totally inhibited by brilliant blue G. These results led us to conclude that basolateral P2X4-like receptors were involved. We suggest that there is a reciprocal purinergic system acting both at a basolateral and apical location for control of Na+ transport. This requires a mechanism within the cell that leads to either basolateral or apical ATP release to regulate renal tubular function.




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