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Am J Physiol Renal Physiol 264: F899-F906, 1993;
0363-6127/93 $5.00
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AJP - Renal Physiology, Vol 264, Issue 5 899-F906, Copyright © 1993 by American Physiological Society

ARTICLES

Enhanced HCO3 secretion by distal tubule contributes to NaCl-induced correction of chronic alkalosis

D. E. Wesson and G. M. Dolson
Veterans Affairs Medical Center, Houston, Texas 77030.

Free-flow micropuncture studies show depressed net HCO3 reabsorption in the surface distal tubule of rats undergoing correction of chronic metabolic alkalosis induced by NaCl infusion. The present studies used in vivo microperfusion of the rat distal tubule to investigate whether the described reduction in net HCO3 reabsorption was due to decreased luminal H+ secretion or to increased HCO3 secretion. Animals with correcting alkalosis had higher HCO3 secretion in this nephron segment than did animals with maintained alkalosis regardless of whether the perfusing solution was initially Cl free (-27.6 vs. -16.6 pmol.mm-1.min-1, P < 0.01) or contained 40 mM Cl (-31.5 vs. -23.0 pmol.mm-1.min-1, P < 0.01); H+ secretion was not different between animals with correcting and maintained alkalosis. Animals without alkalosis (control) demonstrated no differences in H+ or HCO3 secretion in response to NaCl infusion. These studies demonstrate that enhanced HCO3 secretion mediates the depressed net HCO3 reabsorption observed in the distal tubule of rats undergoing NaCl-induced correction of chronic metabolic alkalosis.


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Regulated expression of pendrin in rat kidney in response to chronic NH4Cl or NaHCO3 loading
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[Abstract] [Full Text] [PDF]


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