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Am J Physiol Renal Physiol (October 30, 2001). doi:10.1152/ajprenal.00147.2001
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Articles in PresS, published online ahead of print October 30, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00147.2001
Submitted on May 10, 2001
Accepted on October 4, 2001

ATP Masks Stretch-Activation of Epithelial Sodium Channels in A6 Distal Nephron Cells

He-Ping Ma1*, Li Li1, Zhen-Hong Zhou1, Douglas C Eaton2, and David G Warnock1

1 Department of Medicine, Division of Nephrology, University of Alabama at Birmingham, Birmingham, Alabama, none
2 Department of Physiology, Center for Cell and Molecular Signaling, Emory University School of Medicine, Atlanta, Georgia, none

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

The mechanosensitivity of ENaC is controversial. Using cell-attached patch-clamp techniques, we found that mechanical stretch stimulated ENaC in A6 distal nephron cells in only 3 out of 9 cell-attached patches. However, stretch consistently activated ENaC after apical ATP was scavenged with apical hexokinase plus glucose, or after blocking P2 receptors in the patch. The mean open probability (Po) of ENaC was increased from 0.31 ± 0.04 to 0.61 ± 0.06 (P < 0.001; n = 9) when patch pipettes contained hexokinase and glucose, or from 0.24 ± 0.05 to 0.55 ± 0.11 (P < 0.01; n = 7) when patch pipettes contained suramin, respectively. A poorly hydrolyzable ATP analog, ATP{gamma}S, in the patch pipettes inhibited ENaC, reducing the Po from 0.41 ± 0.06 to 0.19 ± 0.05 (P < 0.01, n = 8). Pretreatment of A6 cells with the phospholipase C (PLC) inhibitor, U-73122, abolished the effect of ATP on ENaC activity. These data together suggest that ATP acting through a PLC-dependent purinergic pathway masks stretch-induced ENaC activation.




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