help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gard, T. G.
Right arrow Articles by Larsen, P. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gard, T. G.
Right arrow Articles by Larsen, P. R.

Endocrinology, Vol 108, 2046-2053, Copyright © 1981 by Endocrine Society


ARTICLES

Studies on the mechanism of 3,5,3'-triiodothyronine-induced suppression of secretagogue-induced thyrotropin release in vitro

TG Gard, B Bernstein and PR Larsen

A double column perifusion procedure was used to study the feedback inhibition of L-T3 on TSH secretion from rat anterior pituitary fragments. Matching pituitary halves were pretreated with T3 (10(-7) M) for 2 h before exposure to 10(-8) M TRH, 59 mM K+, or 5 mM Ba2+ . TRH, high K+, and Ba2+ resulted in a 2-fold or greater stimulation of TSH release. T3 significantly inhibited the stimulation by these secretagogues to 0.77, 0.78, and 0.52 of control for TRH, high K+, and Ba2+, respectively. Neither rT3 (10(-7) M) nor T3 added together with TRH had an effect on TSH release by this secretagogue. Perifusion with 3.5 x 10(-5) M cycloheximide or 10(-6) M actinomycin D 1 h before and during T3 administration led to greater TSH release with TRH than in the presence of T3 alone. Neither protein synthetic inhibitor increased TRH responsiveness of pituitary fragments when perifused alone. When cycloheximide was perifused in a similar protocol before high K+ or Ba2+, there again was a significant decrease in the T3-induced inhibition of TSH release by these secretagogues. Cycloheximide alone did not increase TSH release in response to high K+ or Ba2+, eliminating this as a possible explanation for the enhanced TSH response when antibiotic was present with T3. These results indicate that the in vitro effect of T3 on secretagogue-induced TSH release can be blocked by an inhibitor of protein synthesis. The inhibitory effect of T3 on high K+- and Ba2+-induced TSH release suggests that the site of the acute T3 inhibition of TSH release may be subsequent to TRH interaction with its receptor.


This article has been cited by other articles:


Home page
EndocrinologyHome page
S.-W. Kim, J. W. Harney, and P. R. Larsen
Studies of the Hormonal Regulation of Type 2 5'-Iodothyronine Deiodinase Messenger Ribonucleic Acid in Pituitary Tumor Cells Using Semiquantitative Reverse Transcription-Polymerase Chain Reaction
Endocrinology, December 1, 1998; 139(12): 4895 - 4905.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1981 by The Endocrine Society