Effects of osmotic diuresis on sodium reabsorption and oxygen consumption of kidney

Abstract

Filtered and excreted Na and renal O2 consumption were measured simultaneously in anesthetized dogs undergoing diuresis induced by water or Ringer solution (control), mannitol, and ethacrynic acid. Under control conditions the regression of total renal O2 consumption, VO2, on net Na reabsorption, TNa, was: VO2= 0.034 (SE 0.005) TNa + 0.013 (SE 0.045), indicating a Na/O2 ratio of 29 Eq Na/mold O2, SE 3. Mannitol diuresis decreased TNa 34%; but Vo2 was not affected. Further reduction of TNa during sustained mannitol diuresis by elevation of ureteral pressure or by hemorrhage indicated a new regression of VO2 on TNa : VO2 = 0.051 (.006) TNa + 0.042 (0.023). Na/O2 apparently decreased to 20 Eq Na/mole O2 [plus or minus] 3. Low Na/O2 was not considered due to heterogeneity of Na/O2 between proximal and distal epithelium since selective blockade of distal Na reabsorption by ethacrynic acid did not affect the normal Na/O2. Increased thermodynamic work of Na transport would decrease Na/O2 uniformly in both proximal and distal tubules, or there could be active reabsorption of a nonmeasurable quantity of Na that enters tubular fluid by net inward diffusion during osmotic diuresis, causing an apparent but not real decrease in Na/O2-Though anatomical localization of such Na cycling is not possible at present, the thick ascending limb of Henle''s loop is considered a likely site of extra-active Na transport. Thus, the latter theory implicates the outer medulla as a site of greatly increased O2 utilization during osmotic diuresis.