Figure 1.

In the CCD during reduced Cl⁻ delivery to that segment in CDA, pendrin activity is increased but secretion of HCO₃⁻ is inhibited by insufficient Cl^- for anion exchange. HCO₃⁻ reabsorption may be partly maintained by Na⁺/H⁺ exchange by the electrical coupling between the principal cell and the H⁺-secreting A cell (although it is morphologically less active than normal¹⁷) and by the remainder of the collecting duct in the medulla. Coupled Na⁺/K⁺ exchange causes kaliuresis. After Cl⁻ delivery to the cortical collecting ducts increases, HCO₃⁻ secretion occurs and medullary HCO₃⁻ reabsorption diminishes,³² allowing correction of the hypochloremic alkalosis. In our rat studies, bicarbonaturia occurred within minutes of Cl⁻ administration intravenously and Cl⁻ did not increase in the urine until correction of serum [Cl⁻] was nearly complete. (Both H⁺ and HCO₃⁻ are produced in the A- and B-type cells by carbonic anhydrase, and during acute acid-base changes, pendrin and H⁺ ATPase shuttle back and forth from cytosol to the luminal or basolateral membrane¹⁸).