Abstract

Intact mouse thyroid glands were used to measure the formation of cyclic [3H]AMP from [3H]adenine, and the release of thyroidal iodine. These two parameters of thyroid activity responded to similar concentrations of thyroid-stimulating hormone (TSH). Both were stimulated by prostaglandin E1, although the response was always very much less than to TSH. Both were inhibited by NaF, which appeared to have a toxic effect on the gland. The response to TSH was in each case reduced by lithium, suggesting that the antithyroid effect of Li+ is associated with a direct action on adenyl cyclase; however, Li+ also reduced thyroidal hormone secretion induced by dibutyryl cyclic AMP and may therefore have a second site of action. In general, the effects of these agents on cyclic [3H]AMP formation correlated well with their effects on thyroidal iodine release. The results support the hypothesis that the activation of adenyl cyclase is closely associated with, and precedes, thyroid hormone secretion.

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