Renal tissue hypoxia is a key contributor to the progression of chronic kidney disease (CKD), which occurs in more than 50% of patients with obstructive sleep apnoea (OSA). OSA is characterized by repetitive cycles of intermittent hypoxia (IH) causing oxidative stress. However,the impact of acute and chronic IH on renal function and O2 homeostasis is unclear. Male Sprague Dawley rats (8-10 weeks old) were exposed to IH (270 secs @ 21% O2; 90 secs @ 6.5% O2 at nadir) for 4 hrs in plethysmography chambers (AIH) (n=7) and for 8hrs/day for 2wks in an oxycyclerTM environmental chamber (n=7,CIH). Sham animals were exposed to normoxia under similar conditions (n=6 for AIH study and n=7 for CIH study). Animals were anesthetized (Euthatal:60mg/kg IP) and surgically prepared for the measurement of mean arterial pressure (MAP), left renal excretory function, renal blood flow (RBF) (transonic flow probe), and oxygen tension (PO2) in the renal cortex (C) and medulla (M) (fluorescence quenching oximetry). Animals were euthanized by anesthetic overdose at the end.Data: 2X2 (gas x duration) ANOVA with P<0.05 taken as significant. AIH had no effect on MAP (123±6 (mean±SEM) versus (v) 129±5mmHg), whereas animals exposed to CIH were hypertensive (122±3 v 144±6mmHg (P<0.05). AIH heightened glomerular filtration rate (GFR) (0.92±0.11 v 1.33±0.13ml/min), (RBF) (3.8±0.6 v 7.2±0.9ml/min) and transported sodium (TNa) (132±16 v 201±18μmol/min) (all P<0.05). Conversely, CIH had the opposite effect, reducing GFR (1.15±0.09 v 0.86±0.11ml/min (P=0.06)), RBF (4.13±0.61 v 3.08±0.57ml/min (P<0.05)) and TNa (160±13 v 120±15μmol/min (P<0.05)) (Interaction: P<0.05). Oxygen consumption (QO2) was elevated by AIH (6.76±1.06 v 13.60±2.93μmol/min) (p<0.05) but was not significantly altered by CIH (3.97±0.69 v 6.82±1.24μmol/min). CPO2 was unaltered by AIH (46±1 v 46±1mmHg) but was reduced by CIH (44±3mmHg v 38±1mmHg (p<0.05)). MPO2 was not altered by either AIH (21±1 v 23±1mmHg) or CIH (18±1 v 21±1mmHg). The metabolic consequences of heightened RBF and GFR in animals exposed to AIH are reflected by corresponding increases in TNa and QO2. The fact that renal PO2 was not altered in conjunction with QO2 indicates that acute IH exposure activates a compensatory mechanism in the kidney whereby O2 delivery (RBF) and QO2, although elevated remain balanced, thereby preserving tissue O2 availability. Interestingly, CIH had the opposite effect on RBF and GFR and the metabolic consequences of a diminished GFR are reflected by corresponding reductions in TNa but not in QO2, which even tended to be increased. These observations indicate that transport independent QO2 might well be heightened in response to CIH. Importantly, this apparent inefficiency of QO2 for TNa, coupled with a reduction in O2 delivery most likely accounts for the cortical hypoxia observed in animals exposed to CIH.