Literature DB >> 2484839

Red cell sodium and ionic fluxes in patients with hyper- and hypothyroidism.

Y S Yoon, K S Hong, B Y Cha, Y W Kim, K W Lee, H Y Son, S K Kang, B K Bang, H R Moon.   

Abstract

To investigate the status of the Na+ concentrations [Na+]i, K+ concentrations [K+]i and ionic fluxes in red cells of human subjects with abnormal thyroid function, we measured the Na(+)-K+ pump activity as well as Na(+)-K+ cotransport (CoT), Na(+)-Li+ countertransport (CTT) and Na+ passive permeability in erythrocytes of 37 normal subjects, 19 untreated hyperthyroid patients, 12 treated hyperthyroid patients and 9 hypothyroid patients with T4 replacement. The mean [Na+]i value in the untreated hyperthyroidism group was significantly higher than that in the normal subjects (p less than .05), but not significantly different from that in the treated hyperthyroidism group. The mean [Na+]i value in the hypothyroidism with T4 replacement group, however, was significantly lower than that in the normal group (p less than .01). We did not find any significant difference of [K+]i in comparing each group. It was found that the Na(+)-K+ pump activity in erythrocytes was significantly increased in untreated hyperthyroidism (mean; 23.4% above control, p less than 10(-5], but there was no significant difference in treated hyperthyroidism and hypothyroid patients with T4 replacement. The rate constant for ouabain-sensitive Na+ efflux in the hypothyroidism with T4 replacement group was markedly higher than that in normal subjects (p less than .01), but not significantly different in the untreated hyperthyroidism group. We observed a significant increase of the Na+ CoT value in the patients with untreated hyperthyroidism as compared with that of the normal subjects (p less than .05), but there was no significant difference in the patients treated for hyperthyroidism and the hypothyroidism with T4 replacement group. However, the rate constant for Na(+)-CoT in the patients with hypothyroidism with T4 replacement was significantly higher than that in normal subjects (p less than .05). We observed a marked decrease of Na(+)-Li+CTT value in the patients with untreated hyperthyroidism versus that in the normal group (p less than .01). Passive Na+ permeability in the patients with untreated hyperthyroidism was markedly increased (p less than .05), and was markedly decreased in the patients with hypothyroidism with T4 replacement compared to normal subjects (p less than .01). It can be concluded from these studies that an increase in Na(+)-K+ pump activity in the patients untreated for hyperthyroidism might then be regarded as a secondary adaptive cellular response to higher [Na+]i values due to enhanced passive Na+ permeability, rather than a direct effect of the thyroid hormone.

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Year:  1989        PMID: 2484839      PMCID: PMC4534973          DOI: 10.3904/kjim.1989.4.1.18

Source DB:  PubMed          Journal:  Korean J Intern Med        ISSN: 1226-3303            Impact factor:   2.884


  24 in total

1.  Thyroid calorigenesis in isolated, perfused rat liver: minor role of active sodium-potassium transport.

Authors:  M Folke; L Sestoft
Journal:  J Physiol       Date:  1977-07       Impact factor: 5.182

Review 2.  Thyroid thermogenesis.

Authors:  I S Edelman
Journal:  N Engl J Med       Date:  1974-06-06       Impact factor: 91.245

3.  Time-course of the effects of thyroid hormone on respiration and Na+ + K+-ATPase activity in rat liver.

Authors:  F Ismail-Beigi; I S Edelman
Journal:  Proc Soc Exp Biol Med       Date:  1974-09

4.  Effects of thyroid status on electrolyte distribution in rat tissues.

Authors:  F Ismail-Beigi; I S Edelman
Journal:  Am J Physiol       Date:  1973-11

5.  Mechanism of thyroid calorigenesis: role of active sodium transport.

Authors:  F Izmail-Beigi; I S Edelman
Journal:  Proc Natl Acad Sci U S A       Date:  1970-10       Impact factor: 11.205

6.  Thyroid hormones and the energetics of active sodium-potassium transport in mammalian skeletal muscles.

Authors:  R Biron; A Burger; A Chinet; T Clausen; R Dubois-Ferrière
Journal:  J Physiol       Date:  1979-12       Impact factor: 5.182

7.  Thyroid hormone control of Na+-K+-ATPase and K+-dependent phosphatase in rat heart.

Authors:  K D Philipson; I S Edelman
Journal:  Am J Physiol       Date:  1977-05

8.  Increased (Na+,K+)-ATPase concentrations in various tissues of rats caused by thyroid hormone treatment.

Authors:  M H Lin; T Akera
Journal:  J Biol Chem       Date:  1978-02-10       Impact factor: 5.157

9.  Thyroid-induced alterations in myocardial sodium-potassium-activated adenosine triphosphatase, monovalent cation active transport, and cardiac glycoside binding.

Authors:  G D Curfman; T J Crowley; T W Smith
Journal:  J Clin Invest       Date:  1977-03       Impact factor: 14.808

10.  The mechanism of the calorigenic action of thyroid hormone. Stimulation of Na plus + K plus-activated adenosinetriphosphatase activity.

Authors:  F Ismail-Beigi; I S Edelman
Journal:  J Gen Physiol       Date:  1971-06       Impact factor: 4.086

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