EFFECT OF ACTINOMYCIN-D ON TSH FORMATION RELEASE AND INHIBITION BY THYROXIN

Actinomycin-D, in doses known to block the metabolic effects of thyroid hormone, failed to alter the circulating TSH titer of hypothyroid rats and the rate of disappearance of TSH from the circulation in euthyroid and hypothyroid rats. It also failed to depress the marked increase in pituitary TSH content seen after thyroxin injection into hypothyroid rats. Unexpectedly, actinomycin-D alone caused an increase in pituitary TSH and inhibited the ability of thyroxin to suppress TSH secretion. Therefore, it is suggested that there may be an intrahypophyseal repressor substance which tonically limits TSH formation and is dependent upon a short-lived messenger-RNA which is blocked by actinomycin-D. Possibly this intrahypophyseal repressor is the intermediary by which thyroid hormone inhibits the pituitary. Actinomycin-D, at a concentration as low as 0.056 μg/ml, also inhibited the osmoregulatory response of thyroid slices to TSH stimulation in vitro. © 1968.