Advertisement
Research Article Free access | 10.1172/JCI105510
Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas
†Address requests for reprints to Dr. Floyd C. Rector, Jr., Dept. of Internal Medicine, University of Texas Southwestern Medical School, 5323 Harry Hines Blvd., Dallas, Texas 75235.
‡Work performed during the tenure of a postdoctoral fellowship of the U. S. Public Health Service, grant I-F 2-AM-28, 784-01.
§Work performed as a trainee of the U. S. Public Health Service, grant 5 TI HE 5469-04.
*Submitted for publication May 31, 1966; accepted September 22, 1966.
This work was supported in part by a grant from the Dallas Heart Association and in part by training grant 5 TI HE 5469-04 from the National Institutes of Health, U. S. Public Health Service.
Find articles by Rector, F. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas
†Address requests for reprints to Dr. Floyd C. Rector, Jr., Dept. of Internal Medicine, University of Texas Southwestern Medical School, 5323 Harry Hines Blvd., Dallas, Texas 75235.
‡Work performed during the tenure of a postdoctoral fellowship of the U. S. Public Health Service, grant I-F 2-AM-28, 784-01.
§Work performed as a trainee of the U. S. Public Health Service, grant 5 TI HE 5469-04.
*Submitted for publication May 31, 1966; accepted September 22, 1966.
This work was supported in part by a grant from the Dallas Heart Association and in part by training grant 5 TI HE 5469-04 from the National Institutes of Health, U. S. Public Health Service.
Find articles by Sellman, J. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas
†Address requests for reprints to Dr. Floyd C. Rector, Jr., Dept. of Internal Medicine, University of Texas Southwestern Medical School, 5323 Harry Hines Blvd., Dallas, Texas 75235.
‡Work performed during the tenure of a postdoctoral fellowship of the U. S. Public Health Service, grant I-F 2-AM-28, 784-01.
§Work performed as a trainee of the U. S. Public Health Service, grant 5 TI HE 5469-04.
*Submitted for publication May 31, 1966; accepted September 22, 1966.
This work was supported in part by a grant from the Dallas Heart Association and in part by training grant 5 TI HE 5469-04 from the National Institutes of Health, U. S. Public Health Service.
Find articles by Martinez-Maldonado, M. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas
†Address requests for reprints to Dr. Floyd C. Rector, Jr., Dept. of Internal Medicine, University of Texas Southwestern Medical School, 5323 Harry Hines Blvd., Dallas, Texas 75235.
‡Work performed during the tenure of a postdoctoral fellowship of the U. S. Public Health Service, grant I-F 2-AM-28, 784-01.
§Work performed as a trainee of the U. S. Public Health Service, grant 5 TI HE 5469-04.
*Submitted for publication May 31, 1966; accepted September 22, 1966.
This work was supported in part by a grant from the Dallas Heart Association and in part by training grant 5 TI HE 5469-04 from the National Institutes of Health, U. S. Public Health Service.
Find articles by Seldin, D. in: JCI | PubMed | Google Scholar
Published January 1, 1967 - More info
The mechanism by which expansion of extracellular fluid volume with isotonic saline suppresses reabsorption in the proximal tubule was studied in rats by examining the relations among glomerular filtration rate (GFR), absolute and fractional reabsorption of filtrate, intrinsic reabsorptive capacity (rate of reabsorption per unit tubular volume), transit time, and tubular volume.
Saline infusions reduced the per cent of the glomerular filtrate reabsorbed in the proximal tubule from 50% during antidiuresis to 25% during saline diuresis. The suppression of proximal reabsorption was the result of two factors: 1) a 30% reduction of intrinsic reabsorptive capacity, and 2) a 26% reduction of tubular volume per unit GFR.
GFR invariably rose during saline diuresis. However, prevention of the rise in GFR by aortic clamping had no effect on either the inhibition of intrinsic reabsorptive capacity or the reduction in tubular volume per unit GFR produced by saline infusions. Expansion of extracellular fluid volume with isotonic saline, therefore, depressed intrinsic reabsorptive capacity and tubular volume per unit GFR by some mechanism completely independent of GFR.
The effects of furosemide administration were contrasted with those of saline infusions. Furosemide inhibited intrinsic reabsorptive capacity by 40% but had no significant effect on proximal fractional reabsorption. The failure to suppress fractional reabsorption was the consequence of a disproportionate rise in tubular volume (relative to GFR) that was sufficient to completely overcome the inhibition of intrinsic reabsorptive capacity. Inhibition of intrinsic reabsorptive capacity alone, therefore, will not result in a net suppression of reabsorption of filtrate in the proximal tubule. We concluded that, although intrinsic reabsorptive capacity was inhibited during saline diuresis, the critical factor responsible for translating this inhibition into effective net suppression of proximal reabsorption was the observed reduction in tubular volume per unit GFR.