Effect of hypoxia on renal flow.

The isolated perfused rat kidney was used to characterize the renal response to hypoxia while flow was maintained. Hypoxia resulted in an 85% reduction in glomerular filtration rate (GFR) without any change in total renal vascular resistance. There was an initial 85% increase in urine flow rate (UV) and a 45% decrease in percent sodium reabsorption due to hypoxic metabolic inhibition of solute reabsorption. As GFR decreased, UV declined to 50% of control. GFR did not increase on reoxygenation. These results suggest that an intrinsic protective tubuloglomerular feedback mechanism is activated during hypoxia that redistributes intrarenal flow to reduce the filtered load and to reduce oxygen demand for solute reabsorption. Delivery of oxygen to the hypoxia-sensitive medulla would also be improved. Decreases in GFR observed with ischemic models of acute renal failure may reflect this protective mechanism in addition to the effects of ischemic injury.