K DEPLETION STIMULATES IN-VIVO HCO3 REABSORPTION IN SURVIVING RAT DISTAL TUBULES

To evaluate whether K depletion enhances in vivo bicarbonate reabsorpt ion (J(tCO2)) in surviving distal tubules (DT), we compared DT J(tCO2) in five-sixths nephrectomized rats (Nx) with and without dietary K de pletion (Nx-K). Furthermore, to identify possible mechanisms of increa sed J(tCO2), we perfused inhibitors of proton secretion in both Nx and Nx-K rats. J(tCO2) (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 x 10(-9) M concanamycin A perfusion significantl y decreased J(tCO2) 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. Accor dingly, these combined studies confirm that K depletion enhances J(tCO 2) in surviving DT by stimulating H+-ATPase activity, independent of t he AT(1) receptor.