Abstract
The relationship between changes in tubular sodium reabsorption and changes in renal oxygen consumption (Na/O2) was determined in dogs made anemic, as the arteriovenous difference in oxygen saturation was more than doubled by antecedent bleeding. Tubular sodium reabsorption was reduced by 45 ± 3%, and oxygen consumption by 36 ± 4% after blocking distal sodium transport with ethacrynic acid and chlorothiazide. On the basis of these data it could be calculated that 34 ± 5 Eq Na+ were transported in the distal nephron per/mol O2 consumed. Similar Na/O2 ratios were obtained by reducing proximal sodium reabsorption by lowering glomerular filtration rate after blocking distal sodium reabsorption. During infusion of chlorothiazide and ethacrynic acid, oxygen consumption was not further decreased by reduction of net proximal sodium reabsorption with mannitol infusion. This observation supports the hypothesis that energy-dependent sodium reabsorption in the proximal tubules is not reduced during mannitol diuresis. Na/O2 was not affected by angiotensin in doses which halved renal blood flow, or by sodium sulphate or ferrocyanate in doses raising serum sodium by 40–50 mEq/L. The results are consistent with similar stoichiometric relationships between sodium reabsorption and oxygen consumption in the proximal and parts of the nephron.