Micropuncture study of acidification during hypochloremic alkalosis in the rat

Summary

Hypochloremic alkalosis (HA) was induced in rats through NaCl depletion by furosemid administration and subsequent maintenance on a low-Cl diet supplemented with sodium and potassium bicarbonate. Marked hypochloremia and alkalosis were obtained. Proximal tubular chloride TF/P was 1.35, as high as in controls; lower chloride ratios were found only in final urine. Increased segmental chloride reabsorption was also found only along the collecting duct, leading to lower fractional excretion than in controls. pH and bicarbonate concentration along the nephron, measured by the antimony microelectrode, were considerably elevated, though not as much as in acute bicarbonate loading. Bicarbonate reabsorption per ml GFR was greater in HA up to the early distal tubule both than in controls and in acute alkalosis. The latter condition showed a higher fractional excretion rate of bicarbonate than HA in spite of similar filtered loads. Microperfusion studies with bicarbonate containing solutions showed reduced capacity of the proximal tubular wall to maintain pH and bicarbonate gradients in HA. CO₂ equilibration and bicarbonate disappearance half-times were not much changed. Bicarbonate reabsorptive rates in HA at the elevated concentrations found along the proximal tubule were equal or higher than in controls.