Studies on the Mechanism of the Inhibitory Action of Excess Iodide on the Release of Radioiodine from the Rat Thyroid Gland

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Abstract
Thyroid release of radioiodine was inhibited by excess iodide in rats receiving a small daily dose of propylthiouracil (PTU). This inhibition by excess iodide is not due to the synthesis and release of unlabeled thyroid hormone in amounts adequate to inhibit the release of thyrotropin, for the dilution of 131i within the thyroid by newly formed organic I after excess iodide is the same in the groups which received either a small (5 mg) or a large (30 mg) dose of PTU. Furthermore, the amount of plasma PBI [protein-bound iodine] newly secreted is negligible at both levels of PTU. Demonstration of the iodide effect in thyroxine and TSH [thyroid-stimulating hormone] treated animals indicated further that the iodide effect was not due to inhibition of TSH secretion. Administration of a small dose of PTU immediately augmented release of radioiodine from the thyroid, increased blood TSH within 24 hr. and produced a large goiter after 2 weeks. Large doses of PTU are less effective in these actions. Administration of a small dose of methimazole similarly augments thyroid release of radioiodine with a 9 hr. latency and increases blood TSH within 36 hr. Since the iodide effect can be seen in animals treated with methimazole, and since iodide manifests its effect at the level of the thyroid, small doses of PTU and methimazole play an important role in producing the iodide effect by augmenting the pituitary release of TSH and thereby the uptake of iodide.