Phorbol Myristate Acetate Inhibits α1-Adrenergically but Not Thyrotropin-Regulated Functions in FRTL-5 Rat Thyroid Cells

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Abstract
The iodination of thyroglobulin and the formation of thyroid hormones are regulated by .alpha.1-adrenergic agents as well as TSH in rat FRTL-5 cells. The regulatory effects of the .alpha.1-adrenergic agents and TSH on both of these processes are associated with an increase in cytosolic Ca2+ and an increase in that components of iodide efflux that is representative of the movement of iodide from the thyroid cell into the follicular lumen. When FRTL-5 cells are preincubated with phorbol myristate acetate (PMA) for at least 3 min, the norepinephrine-stimulated changes in cytosolic Ca2+ levels and iodide efflux are inhibited. In contrast, PMA pretreatment has no effects on iodide efflux and actually enhances the changes in cytosolic Ca2+ induced by TSH. Phorbol myristate acetate pretreatment has no effect on TSH-stimulated cAMP-mediated iodide uptake in FRTL-5 cells, nor does it affect the binding parameters of the .alpha.1-adrenergic receptor antagonist prazosin. These data suggest 1) that protein kinase C is involved in a feedback mechanism regulating .alpha.1-adrenergic but not TSH-induced changes associated with the iodination of thyroglobulin and the formation of thyroid hormones; and 2) that this feedback effect occurs after the step of ligand binding but before the increase in cytosolic Ca2+ induced by the .alpha.1-adrenergic agents.
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