THYROTROPIN-INDUCED RELEASE OF IODIDE FROM THE THYROID1

Abstract

The early effects of thyrotropin on the iodine metabolism of the dog thyroid were studied by measuring plasma concentrations of stable and radioactive iodine in arterial and thyroid venous blood, 2 to 4 hours after I¹³¹ administration. When organic binding of iodide was not prevented, TSH administration led to the prompt release from the gland of TCA-soluble as well as TCA-precipitable stable iodine with relatively little change in the glandular clearance of circulating labeled iodide; iodide release was considerably enhanced by perchlorate. When organic binding was blocked (methimazole) TSH led to the release of both stable and radioactive iodide from the gland and the released iodide was of lower specific activity than arterial iodide. The data suggest that TSH enhances the formation of iodide in the gland, probably by deiodination of organic iodine compounds (iodotyrosines). The iodide so produced seemed to be at least partially exchangeable with circulating iodide concentrated by the gland when organic binding was blocked, but when binding was permitted there was little evidence of such exchange during a relatively short period of observation. When organic binding was not prevented, the administration of perchlorate to both TSH-injected and control animals led to glandular release of iodide of specific activity considerably less than that of circulating iodide, suggesting the presence within the thyroid of iodide poorly exchangeable with iodide newly entered from the circulation.