Effects of d-Propranolol Treatment on Transport of Thyroid Hormones into Tissue Cells

  • Roelof Docter
  • Johannes T. M. van der Heijden
  • Eric P. Krenning
  • Georg Hennemann


It is well known that treatment with d,1-propranolol elicits a low T3 syndrome in man (1,2). This has been explained by the assumption of an inhibition of 5’-deiodinase in the liver by d,l-propranolol, leading to a diminished production of T3 from T4 and a diminished breakdown of rT3. However, the Ki of d,l-propranolol on this enzyme in vitro is about 0.8 mM (3), (3), while therapeutic levels of this compound are between 0.5 and 1 µM in serum (4), and, at least in the rat, the liver does not concentrate propranolol (5). Recently, it has been shown that a derivative, 4-OH-propranolol, markedly inhibits 5’-deiodinase activity in vitro at a concentration of about 50 µM (6), but the concentration in serum is below 50 nM (6). Inhibition of the enzyme in vivo seems, therefore, questionable. On the other hand, we have found that transport of iodothyronines into rat liver hepatocytes in primary culture is strongly inhibited by propranolol in a concentration of only 1 µM (7). Furthermore, we have shown that at least part of the low T3 syndrome, elicited by caloric deprivation, can be attributed to inhibition of transport of T4 into the liver (8). Therefore, we have performed tracer T4, T3, and rT3 kinetic studies to investigate if the low T3 syndrome elicited by propranolol is caused by transport inhibition of T4 and rT3 into the liver, or by inhibition of conversion of T4 to T3 and rT3 to T2.


Mass Transfer Rate Propranolol Treatment Deiodinase Activity Slow Pool Caloric Deprivation 
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Copyright information

© Springer Science+Business Media New York 1986

Authors and Affiliations

  • Roelof Docter
    • 1
  • Johannes T. M. van der Heijden
    • 1
  • Eric P. Krenning
    • 1
  • Georg Hennemann
    • 1
  1. 1.Dept. of Internal Medicine III and Nuclear MedicineErasmus UniversityRotterdamThe Netherlands

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