Mechanism of the Suppression by Iodide of the Thyroidal131I Release Rate in the Rat

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Abstract
Yamada et al. reported that the administration of KI decreased the thyroidal I131 release rate of the rats receiving moderate doses of propylthiouracil (PTU) (5 mg/day or less) to block recycling of radioiodide. It had no effect when the rats received 30 mg PTU/day, though the half-life of thyroidal I131 was the same in both cases. These findings are confirmed here. It is moreover shown that in the 1st case the injection of KI results in an increased synthesis of iodothyronines, but not in the case of rats on the higher PTU doses. Estimation of thyroidal I131 release rates, intrathyroidal I127 distribution among I-containing compounds, plasma PBI [protein-bound iodine] and plasma and pituitary TSH [thyroid-stimulating hormone] activities in animals receiving an injection of stable iodide while the thyroid was being blocked with CIO4- or with PTU support the following interpretations: The thyroidal Il3l release rate of rats receiving either high or low doses of PTU reflects an intensely increased, and not a normal, degree of TSH stimulation. The injection of stable iodide induces an increase in the synthesis of iodothyronines when the block exerted by PTU is not complete. The amount of hormonal iodine then released is high enough to counteract the TSH-releasing effects of PTU. The decrease in circulating TSH is then reflected by a decline of the previously accelerated rate of thyroidal I131 release. This would not occur when the block exerted by PTU effectively avoids synthesis of iodothyronines after injection of stable iodide. An unexpected and as yet not adequately explained finding was that the entry of stable iodide into glands inefficiently blocked with CIO4-PTU or Tapazole was accompanied by a rearrangement of the distribution of Il3l among thyroidal iodoamino acids consisting in an increase in labeled iodothy-ronines (usually T4) and a decrease in iodotyrosines.