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To find out if the gestation-dependent increase in fetal oncotic pressure is responsible for the gestation-dependent increase in the capacity of the fetal proximal tubule to reabsorb sodium, the effects on renal function of increases in oncotic pressure were studied in 8 volume-expanded chronically catheterized fetal sheep aged 128 +/- 3 (s.e.) days. Fetal extracellular volume was expanded by infusion of 65 +/- 10.8 (s.e.) mliter kg-1 estimated body weight of 0-15 M saline. This caused a decrease in fetal plasma protein concentrations (P < 0.01); fetal oncotic pressure decreased (P < 0.05). A diuresis and natriuresis occurred, which was due not to an increase in glomerular filtration rate but to a decrease in the fraction of the filtered sodium load reabsorbed by the proximal tubule (P < 0.05) and a decrease in the fraction of distally delivered sodium reabsorbed (P < 0.01). Fetal plasma protein concentrations were then increased to greater than control levels (P < 0.01) by infusion of maternal plasma (28 +/- 1.6 mliter kg-1); oncotic pressure was greater than after saline expansion (P < 0.05) and similar to control. The fraction of the filtered sodium load reabsorbed by the proximal tubule remained depressed (P < 0.01) relative to control, as did the fraction of distally delivered sodium that was reabsorbed (P < 0.01). Thus the natriuresis and diuresis continued. There was, however, a small effect of oncotic pressure on proximal fractional sodium reabsorption that was unmasked by multiple regression analysis. Obviously, this effect was not sufficient to override other effects of volume expansion on fetal proximal tubular function. Therefore, the reduction in fetal proximal fractional sodium reabsorption in volume expansion was not due solely to a fall in fetal oncotic pressure. Furthermore, since infusion of maternal plasma caused a rise in fetal plasma protein concentrations that was similar to the increase that would occur between 128 and 148 days gestation, it is unlikely that any gestation-dependent increase in proximal fractional sodium reabsorption is due solely to the increase in fetal plasma protein concentrations and hence oncotic pressure.