Modulation of Pituitary Responsiveness to Throtropin-Releasing Hormone by Triiodothyronine

Louis Shenkman; Terunori Mitsuma; Charles S. Hollander

doi:10.1172/JCI107166

¹Endocrine Unit, Department of Medicine, New York University School of Medicine, New York 10016

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¹Endocrine Unit, Department of Medicine, New York University School of Medicine, New York 10016

Find articles by Mitsuma, T. in: JCI | PubMed | Google Scholar

¹Endocrine Unit, Department of Medicine, New York University School of Medicine, New York 10016

Find articles by Hollander, C. in: JCI | PubMed | Google Scholar

Published in Volume 52, Issue 1 on January 1, 1973
J Clin Invest. 1973;52(1):205–209. https://doi.org/10.1172/JCI107166.
© 1973 The American Society for Clinical Investigation

Published January 1, 1973 - Version history

The relative roles of triiodothyronine (T₃) and thyroxine (T₄) in modulating pituitary responsiveness to thyrotropin-releasing hormone (TRH) have been assessed. (a) 10 hyperthyroid patients with elevated serum T₂ and T₄ levels showed no pituitary response to TRH. After 2 wk of propylthiouracil therapy T₄ levels had fallen to normal in only five patients while T₂ levels were normal in all. Pituitary responsiveness to TRH returned in all patients with normal or high T₄ concentrations. (b) Patients with isolated elevations of serum T₃ (T₃ toxicosis) failed to respond to TRH. TRH responsiveness was restored when T₃ levels fell to normal after propylthiouracil therapy. (c) When pituitary responsiveness to TRH was tested 60 min after a single oral dose of 50 μg of T₃, which increased serum T₃ levels to slightly above the normal range, no rise in thyrotropin (TSH) was seen in six subjects. These findings indicate that T₃ elevations alone can rapidly inhibit pituitary responsiveness to TRH.