The effect of sustained moderate hypoxia on renal blood flow and renal function was studied in the ovine fetus (123-129 days). The experiments consisted of 48 h of isocapnic hypoxia, not resulting in acidemia, but sufficient to produce redistribution of blood flow in favor of the brain at the expense of the carcass. Hypoxemia was induced by maternal nitrogen inhalation. Fetal arterial O₂ saturation and arterial O₂ pressure (Pa_O2) decreased from, respectively, 50.6 ± 3.0% and 17.2 ± 0.9 mmHg during control to 36.4 ± 2.7% and 13.4 ± 0.7 mmHg on the first and to 32.2 ± 2.2% and 12.4 ± 0.7 mmHg on the second day of hypoxemia. Fetal renal blood flow and urine production rate were continuously measured using ultrasonic flow transducers. Fetal renal blood flow increased during hypoxemia from 11.8 ± 1.6 to 15.6 ± 1.8 ml/min and remained elevated throughout the 48-h hypoxemia period (P < 0.01). Renal blood flow was inversely correlated with fetal Pa_O2 (r is 0.69, P < 0.0001). Fetal urine production rate, glomerular filtration rate, filtration factor, osmotic clearance, and free water clearance did not significantly change from control values during hypoxemia or recovery. We conclude that hypoxemia without acidemia results in an immediate and considerable increase in fetal renal blood flow, which remains elevated for the entire hypoxemic period.