Proximal reabsorption during metabolic acidosis in the rat.

The mechanism by which proximal volume reabsorption is reduced during hyperchloremic metabolic acidosis was studied using free-flow micropuncture techniques in Munich-Wistar rats. Compared with control hydropenic conditions, absolute rates of proximal total CO2 and water reabsorption rates during NH4Cl-induced metabolic acidosis were diminished: from 557 +/- 35 to 204 +/- 19 pmol/min and from 13.0 +/- 1.0 to 9.7 +/- 0.6 nl/min, respectively. Inhibition of proximal volume reabsorption during metabolic acidosis was not attributable to alterations in the reabsorptive Starling forces, since peritubular capillary oncotic and hydraulic pressures were normal, or to acidemia itself, since acute respiratory acidosis was not found to decrease reabsorption. When partial repair of the acidosis was achieved by NaHCO3 infusion, absolute reabsorption of both total CO2 (390 +/- 48 pmol/min) and water (12.2 +/- 1.1 nl/min) significantly increased despite modest extracellular volume expansion. NaCl infusion in acidotic animals had no restorative effect on volume reabsorption. Mean values for single nephron glomerular filtration rate were similar under all conditions. Absolute chloride reabsorption tended to correlate better with absolute bicarbonate reabsorption and, hence, with the magnitude of the chloride concentration gradient developed than with the filtered chloride load. In conclusion, absolute proximal volume reabsorption during metabolic acidosis and its partial repair correlated with the absolute magnitude of bicarbonate filtered and reabsorbed. It is proposed that proximal volume reabsorption may be regulated, at least in part, by the anion composition of the glomerular ultrafiltrate.