Renal Na-Reabsorption and O 2 -Uptake in Dogs During Hypoxia and Hydrochlorothiazide Infusion

Abstract

Summary

In anesthetized dogs renal oxygen consumption and sodium reabsorption were determined during hypoxia and under the influence of hydrochlorothiazide. In hypoxia (arterial O₂ saturation 35%) less sodium is reabsorbed and renal O₂ consumption is diminished. Urine volume is increased with a decrease in U/P_osm, U/P_Creat and T^c _H2O. During administration of hydrochlorothiazide both sodium reabsorption and O₂ consumption are lowered. Urine volume and C_osm are elevated, U/P_osm and U/P_Creat decreased while T^c _H2O remains unchanged.

Plotting Na reabsorption (μeq/g min) against O₂ consumption (μmol/g min) results in a straight line which intercepts the O₂ consumption axis at 1 μmol/g min. We believe that this value may be equated with renal basal O₂ consumption; i.e., without Na reabsorption. The O₂ requirement for renal sodium reabsorption is calculated to be 28.6-32 μeq Na/μmol O₂.