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/Posm, U/PCreat and Tc H2O. During administration of hydrochlorothiazide both sodium reabsorption and O2 consumption are lowered. Urine volume and Cosm are elevated, U/Posm and U/PCreat decreased while Tc 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.
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