These experiments examined whether renal growth and the fetal renin-angiotensin system could be stimulated by infusion of amino acids, and if chronic amino acid infusions restored glomerulotubular balance which had been disrupted during 4 hour infusions. Five fetal sheep aged 122 ± 1 days gestation received an infusion of alanine, glycine, proline and serine in 0.15M saline at 0.22 mmol min^-1 for 7 days. Six control fetuses were given saline at the same rate (5 mL h^-1). Kidney wet weights after amino acid infusion were 28% larger than control fetuses (P<0.05) and renal angiotensinogen mRNA levels were approximately 2.6-fold higher (P<0.005). Circulating renin levels and renal renin mRNA levels were suppressed (P<0.05) and renal renin protein levels tended to be lower. Arterial pressure was increased and there was a marked, sustained natriuresis and diuresis. Glomerular filtration rate and filtered sodium were ~2-fold higher throughout infusion (P<0.05). Fractional proximal sodium reabsorption, suppressed at 4 hours (from 73.4 ± 6.5 to 53.7 ± 10.2%), did not return to control levels (36.1 ± 3.4% on day 7, P<0.05). Distal sodium reabsorption was markedly increased (from 79 ± 25 to 261 ± 75 ± µmol min^-1 by day 7, P<0.005), but this was not sufficient to restore glomerulotubular balance. The resultant high rates of sodium excretion led to hyponatremia and polyhydramnios. In conclusion, long term amino acid infusions increased renal angiotensinogen gene expression, kidney weight and distal nephron sodium reabsorptive capacity, but failed to restore proximal and total glomerulotubular balance.