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Provides information on a study that evaluated whether potassium (K) depletion enhances in vivo bicarbonate (HCO3) reabsorption in surviving rate distal tubules (DT). Materials and methods; Effect of K depletion in nephrectomized (Nx) rats; Possible role of other transporters in K-depleted Nx rats; Conclusions.

Distal tubules (DT) from sham or five-sixths nephrectomized (Nx) rats were perfused in vivo to evaluate the hypothesis that, after Nx, endogenous angiotensin II (ANG II) modulates DT in vivo bicarbonate reabsorption (JtCO2 ) via H+-adenosinetriphosphatase (H+-ATPase) and Na+/H+ exchange. In Nx rats JtCO2 was increased (65 ± 7 vs. - 24 ± 21 pmol·min-1·mm-1, P < 0.01). Both luminal and intravenous AT1-receptor blockade by losartan reduced Nx DT JtCO2 (41 ± 6 and 34 ± 4 pmol·min-1·mm-1, respectively, P < 0.05), whereas neither 10-9 M nor 10-11 M ANG II luminal perfusion increased JtCO2, suggesting preexisting high endogenous ANG II levels. The Na+/H+ antiporter inhibitors 5-(iV-ethyl-iV-isopropyl)- amiloride and 5-(A/yV-dimethyl)-amiloride were without effect. Luminal perfusion of 5 nM concanamycin A, a V-type H+-ATPase inhibitor, reduced Nx DT JtCO2 (45 ± 8 pmol · min-1 · mm-1, P < 0.05). In Nx A-type intercalated cells, we demonstrated cellular hypertrophy, elaboration of apical microplicae, and enhanced expression/apical polarization of H+-ATPase. Thus ANG II is an important determinant in sustaining brisk DT JtCO2 following Nx and is associated with enhanced expression ancf A-type intercalated cell apical polarization of H+-ATPase. [ABSTRACT FROM AUTHOR]