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Am J Physiol Renal Physiol 273: F586-F594, 1997;
0363-6127/97 $5.00
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AJP - Renal Physiology, Vol 273, Issue 4 586-F594, Copyright © 1997 by American Physiological Society

ARTICLES

Endothelin-1 increases rat distal tubule acidification in vivo

D. E. Wesson and G. M. Dolson
Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock 79430, USA.

Because endothelin receptor inhibition blunts increased distal tubule acidification induced by dietary acid, we examined whether endothelin-1 (ET-1) increases acidification of in vivo perfused distal tubules of anesthetized rats. ET-1 was infused intraaortically (1.4 pmol x kg(-1) x min[-1]) into control animals and into those with increased distal tubule HCO3 secretion induced by drinking 80 mM NaHCO3 solution for 7-10 days. ET-1 increased distal tubule acidification in both control and NaHCO3 animals. Increased acidification in control animals was mediated by increased distal tubule H+ secretion (23.7+/-2.2 vs. 18.7 +/- 1.7 pmol x mm(-1) x min(-1), P < 0.05) with no changes in HCO3 secretion. By contrast, ET-1 increased distal tubule acidification in NaHCO3 animals predominantly by decreasing HCO3 secretion (-9.5 +/- 1.0 vs. -18.7 +/-1.8 pmol x mm(-1) x min(-1), P < 0.001) with less influence on H+ secretion. When indomethacin was infused (83 microg x kg(-1) x min[-1]) to inhibit synthesis of prostacyclin, an agent previously shown to increase HCO3 secretion in the distal tubule, ET-1 increased distal tubule H+ secretion in both control (24.3 +/-2.2 vs. 15.7 +/- 1.6 pmol x mm(-1) x min(-1), P < 0.02) and NaHCO3 (20.0 +/- 2.0 vs. 13.6 +/- 1.4 pmol x mm(-1) x min(-1), P < 0.05) without affecting HCO3 secretion. The data show that ET-1 increases distal tubule acidification in vivo and can do so by increasing H+ secretion and by decreasing HCO3 secretion when the latter is augmented by dietary NaHCO3.


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