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Free access | 10.1172/JCI106936
Research and Medical Services, Veterans Administration Hospital, Miami, Florida 33125
Department of Medicine, University of Miami, School of Medicine, Miami, Florida 33152
Find articles by Michael, U. in: JCI | PubMed | Google Scholar
Research and Medical Services, Veterans Administration Hospital, Miami, Florida 33125
Department of Medicine, University of Miami, School of Medicine, Miami, Florida 33152
Find articles by Barenberg, R. in: JCI | PubMed | Google Scholar
Research and Medical Services, Veterans Administration Hospital, Miami, Florida 33125
Department of Medicine, University of Miami, School of Medicine, Miami, Florida 33152
Find articles by Chavez, R. in: JCI | PubMed | Google Scholar
Research and Medical Services, Veterans Administration Hospital, Miami, Florida 33125
Department of Medicine, University of Miami, School of Medicine, Miami, Florida 33152
Find articles by Vaamonde, C. in: JCI | PubMed | Google Scholar
Research and Medical Services, Veterans Administration Hospital, Miami, Florida 33125
Department of Medicine, University of Miami, School of Medicine, Miami, Florida 33152
Find articles by Papper, S. in: JCI | PubMed | Google Scholar
Published June 1, 1972 - More info
Hypothyroid rats were examined with conventional renal clearance and micropuncture techniques to elicit the mechanism and site within the nephron responsible for the increased salt and water excretion observed in these animals. When compared with age-matched control rats, a decrease in inulin clearance of 30% (P < 0.001) and in Hippuran clearance of 32% (P < 0.005) was observed in the hypothyroid rats. Absolute excretion of sodium and water was increased 3-fold (P < 0.02) and 2-fold (P < 0.025), respectively, while fractional excretion of sodium and water was increased 4.3-fold (P < 0.02) and 2.9-fold (P < 0.05), respectively, in the hypothyroid animals.
Fractional proximal reabsorption of sodium as assessed from proximal tubular fluid to plasma ratios of inulin ([TF/P]IN) was found to be decreased by 28% (P < 0.001) in the hypothyroid rats. Superficial single nephron filtration rate was reduced proportionately to the decrease in total filtration rate in the hypothyroid rats.
These data indicate that the proximal tubule is one of the sites of diminished sodium and water reabsorption in the hypothyroid rat. The data also suggest that the observed decrease in glomerular filtration rate in the hypothyroid animals is not caused by a decrease in the number of functioning nephrons and that the observed increase in sodium and water excretion is not caused by a redistribution of filtrate from juxtamedullary to superficial nephrons. Although the exact mechanisms of the observed changes in proximal tubular function remain unknown, the data suggest that they are probably related to the lack of thyroid hormone. Whatever their mechanism, it appears that the enhanced sodium and water excretion observed in the hypothyroid animals must be determined by further reduction in tubular sodium reabsorption in the distal nephron.