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Articles in PresS, published online ahead of print April 23, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00379.2001
Submitted on December 28, 2001
Accepted on December 31, 1969
1 Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, NY, USA
* To whom correspondence should be addressed. E-mail: lgpalm{at}med.cornell.edu.
To test the role of epithelial Na channels in the day-to-day regulation of renal Na excretion, rats were infused via osmotic minipumps with the Na channel blocker amiloride at rates which achieved drug concentrations of 2-5 µM in the lumen of the distal nephron. Daily Na excretion rates were unchanged although amiloride-treated animals tended to excrete more Na in the afternoon and less in the late evening compared with controls. When the rats were given a low-Na diet, Na excretion rates were elevated in the amiloride-treated group within 4 hours and remained higher than controls for at least 48 hours. Adrenalectomized animals responded similarly to the low-Na diet. In contrast, rats infused with polythiazide at rates designed to inhibit NaCl transport in the distal tubule were able to conserve Na as well as did the controls. Injection of aldosterone (2 µg/100 g b.w.) decreased Na excretion in control animals after a delay of 1 hour. This effect was largely abolished in amiloride-treated rats. Based on quantitative analysis of the results we conclude that activation of amiloride-sensitive channels by mineralocorticoids accounts for 50-80% of the immediate natriferic response of the kidney to a reduction in Na intake. Furthermore, the channels are necessary to achieve minimal rates of Na excretion during more chronic Na deprivation.
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