Renal Na-Reabsorption and O2-Uptake in Dogs During Hypoxia and Hydrochlorothiazide Infusion

K Thurau - Proceedings of the Society for Experimental …, 1961 - journals.sagepub.com
K Thurau
Proceedings of the Society for Experimental Biology and Medicine, 1961journals.sagepub.com
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 TcH2O. 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 …
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 TcH2O. 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 TcH2O 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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