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Chronic kidney disease (CKD) occurs in more than 50% of patients with obstructive sleep apnea (OSA). However, the impact of intermittent hypoxia (IH) on renal function and oxygen homeostasis is unclear. Male Sprague-Dawley rats were exposed to IH (270 s at 21% O 2 ; 90 s hypoxia, 6.5% O 2  at nadir) for 4 h [acute IH (AIH)] or to chronic IH (CIH) for 8 h/day for 2 wk. Animals were anesthetized and surgically prepared for the measurement of mean arterial pressure (MAP), and left renal excretory function, renal blood flow (RBF), and renal oxygen tension (Po 2 ). AIH had no effect on MAP (123 ± 14 vs. 129 ± 14 mmHg, means ± SE, sham vs. IH). The CIH group was hypertensive (122 ± 9 vs. 144 ± 15 mmHg, P &lt; 0.05). Glomerular filtration rate (GFR) (0.92 ± 0.27 vs. 1.33 ± 0.33 ml/min), RBF (3.8 ± 1.5 vs. 7.2 ± 2.4 ml/min), and transported sodium (TNa) (132 ± 39 vs. 201 ± 47 μmol/min) were increased in the AIH group (all P &lt; 0.05). In the CIH group, GFR (1.25 ± 0.28 vs. 0.86 ± 0.28 ml/min, P &lt; 0.05) and TNa (160 ± 39 vs. 120 ± 40 μmol/min, P &lt; 0.05) were decreased, while RBF (4.13 ± 1.5 vs. 3.08 ± 1.5 ml/min) was not significantly different. Oxygen consumption (QO 2 ) was increased in the AIH group (6.76 ± 2.60 vs. 13.60 ± 7.77 μmol/min, P &lt; 0.05), but it was not significantly altered in the CIH group (3.97 ± 2.63 vs. 6.82 ± 3.29 μmol/min). Cortical Po 2  was not significantly different in the AIH group (46 ± 4 vs. 46 ± 3 mmHg), but it was decreased in the CIH group (44 ± 5 mmHg vs. 38 ± 2 mmHg, P &lt; 0.05). For AIH, renal oxygen homeostasis was preserved through a maintained balance between O 2  supply (RBF) and consumption (GFR). For CIH, mismatched TNa and QO 2  reflect inefficient O 2  utilization and, thereby, sustained decrease in cortical Po 2 .

Renal cortical oxygen tension is decreased following exposure to long-term but not short-term intermittent hypoxia in the rat