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Am J Physiol Renal Physiol 274: F665-F672, 1998;
0363-6127/98 $5.00
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Vol. 274, Issue 4, F665-F672, April 1998

K depletion stimulates in vivo HCO3 reabsorption in surviving rat distal tubules

David Z. Levine1, Michelle Iacovitti1, Susan Buckman1, Brian Luck2, Maxwell T. Hincke2, Kevin D. Burns1, and James N. Fryer2

1 Departments of Medicine and 2 Cellular and Molecular Medicine, University of Ottawa and Ottawa General Hospital, Ottawa, Ontario, Canada K1H 8M5

To evaluate whether K depletion enhances in vivo bicarbonate reabsorption (JtCO2) in surviving distal tubules (DT), we compared DT JtCO2 in five-sixths nephrectomized rats (Nx) with and without dietary K depletion (Nx-K). Furthermore, to identify possible mechanisms of increased JtCO2, we perfused inhibitors of proton secretion in both Nx and Nx-K rats. JtCO2 (102 ± 8 pmol · min-1 · mm-1) was significantly increased in Nx-K vs. Nx rats (65 ± 7 pmol · min-1 · mm-1, P < 0.05) but unaffected by 10-6 M losartan perfusion (94 ± 6 pmol · min-1 · mm-1, P = not significant). Although 10-5 M Sch-28080 also had no significant effect, 5 × 10-9 M concanamycin A perfusion significantly decreased JtCO2 in Nx-K rats to 65 ± 8 pmol · min-1 · mm-1 (P < 0.05). Morphometric evaluation and H+-ATPase immunogold labeling of Nx-K A-type intercalated cells revealed cellular hypertrophy, elaborated apical microplicae, and enhanced H+-ATPase apical polarization. Accordingly, these combined studies confirm that K depletion enhances JtCO2 in surviving DT by stimulating H+-ATPase activity, independent of the AT1 receptor.

kidney failure; receptors; angiotensin; proton-transporting adenosinetriphosphatase; Sch-28080; concanamycin A; net bicarbonate reabsorption


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