Volume expansion modulates NaHCO3 and NaCl transport in the proximal tubule and Henle's loop

The effects of extracellular fluid volume expansion on kidney reabsorption of bicarbonate, chloride, and water were examined in Sprague-Dawley rats by paired micropuncture experiments in which tubular fluid was collected from early distal and end-proximal sites. In group I, rats were studied during a plasma-replete euvolemic state and after 10% body wt colloid-free volume expansion. The filtered loads were similar in euvolemia and expansion; expansion increased end-proximal total CO2 concentration ([tCO2] EP) from 13.0 +/- 0.8 to 18.4 +/- 0.7 mM and inhibited the tCO2 fractional reabsorption 26% in the proximal convoluted tubule and 15% in Henle's loop. Early distal tCO2 delivery therefore increased from 61 +/- 7 to 140 +/- 17 pmol X min-1 X g kidney wt-1. A more pronounced inhibition of fractional reabsorption of chloride (45%) and water (35%) occurred in the proximal convoluted tubule during expansion. In group II, rats were studied during 5% body wt 70 g/liter albumin-containing expansion and after 10% body wt colloid-free expansion. Compared with euvolemia of group I, albumin expansion decreased proximal fractional reabsorption of tCO2 13%, chloride 19%, and water 14% without change in filtered loads, and [tCO2]EP rose to 17.2 +/- 0.7 mM. A 10 g/liter decrease in plasma protein concentration during colloid-free expansion was associated, compared with albumin expansion, with inhibition of proximal fractional reabsorption of tCO2 by 4%, chloride by 18%, and water by 9% without further altering [tCO2]EP. We conclude that 1) expansion specifically inhibits bicarbonate reabsorption in the proximal convoluted tubule and in Henle's loop independent of change in filtered load or in peritubular protein concentration, probably by enhancing bicarbonate backdiffusion and reducing proton secretion; 2) expansion-induced decrease in peritubular protein concentration contributes to the proximal expansion effect probably by specifically inhibiting transcellular sodium chloride reabsorption.