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

To evaluate whether K depletion enhances in vivo bicarbonate reabsorption ([Formula: see text]in surviving distal tubules (DT), we compared DT[Formula: see text]in five-sixths nephrectomized rats (Nx) with and without dietary K depletion (Nx-K). Furthermore, to identify possible mechanisms of increased[Formula: see text], we perfused inhibitors of proton secretion in both Nx and Nx-K rats.[Formula: see text](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[Formula: see text]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[Formula: see text]in surviving DT by stimulating H+-ATPase activity, independent of the AT1 receptor.