These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Effect of sodium intake on single nephron glomerular filtration rate and sodium reabsorption in experimental uremia.
    Author: Weber H, Lin KY, Bricker NS.
    Journal: Kidney Int; 1975 Jul; 8(1):14-20. PubMed ID: 1160221.
    Abstract:
    Sodium balance, clearance and micropuncture studies were performed on three groups of uremic rats in which renal mass was reduced experimentally by approximately 85%. All animals received a sodium-free synthetic diet to which a measured amount of NaCl was added. Sodium intake was 3 mEq/day in one group, 1 mEq/day in a second group and 0.13 mEq/day in the third. In the latter, the Na intake was reduced (from an initial level of 1 mEq/day) as renal mass was reduced in proportion to the estimated reduction in renal mass in an effort to obviate the requirement for an increased natriuresis/nephron. Clearance and micropuncture studies also were performed in a group of normal rats maintained on 1 mEq/day of Na. All three groups of uremic rats on the standard diet maintained external Na balance. Single nephron glomerular filtration rate (SNGFR) in superficial nephrons was increased in all three groups of uremic rats and seemed to be independent of the Na intake; fractional fluid reabsorption was decreased in the proximal tubules in all three groups of uremic rats. Furthermore, absolute proximal Na reabsorption was markedly increased; and calculated values for distal reabsorption were markedly increased in all groups of uremic rats. The data suggest that the increase in SNGFR and the decrease in tubular fluid to plasma (TF/P) inulin ratios in superficial proximal tubules correlate poorly with the dictates for an increase in sodium excretion rate per residual nephron. These data also have implications regarding the operation of the control system in the regulation of external Na balance in uremia.
    [Abstract] [Full Text] [Related] [New Search]