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Dopamine and L-Dopa: inhibition of Thyrotropin-Stimulated Thyroidal Thyroxine Release^*

Nuclear Medicine Department, Veterans Administration Medical Center, and Downstate Medical Center Brooklyn, New York 11209

Address requests for reprints to: Morelly L. Maayan, M.D., Nuclear Medicine Service, Veterans Administration Medical Center, 800 Poly Place, Brooklyn, New York 11209.

Abstract

Previous studies had suggested that norepinephrine (NE) and its precursors dopamine (DA) and L-DOPA acted similarly on iodine metabolism of isolated thyroid cells. Present studies indicate that this similarity extends to the inhibition by catecholamines of TSH-stimulated T4 release by mouse thyroids incubated in vitro. DA (5 x 10^–4 M), like NE, shown previously, inhibits TSH-stimulated T₄ release. This inhibition was reversed by the -blockers phentolamine, prazosin, and yohimbine, but not by the β-blocker L-propranolol. DU-18288 and diethyldithiocarbamate, inhibitors of DA β-hydroxylase, did not reduce DA inhibition, suggesting that prior conversion to NE was not a condition for DA activity. Apomorphine, a dopaminergic agonist but not a NE precursor, acted like DA, and its inhibition was also reversed by -blockers. Furthermore, sulpiride, a dopaminergic blocker, reversed DA and apomorphine inhibition of TSH stimulation. These results suggest that DA inhibits TSH-stimulated T₄ release through both adrenergic and dopaminergic receptors. On the other hand, L-DOPA, exerting an inhibition like that of DA, was also reversed by -blockers, but its activity was greatly diminished by carbidopa, an inhibitor of aromatic L-amino acid decarboxylase, the enzyme converting L-DOPA to DA. This indicated that L-DOPA had to be converted to DA for activity. Both DA and L-DOPA inhibited stimulation of T₄ release induced by (Bu)₂cAMP, suggesting that their effect was exerted at a locus distal to cAMP generation. Indirect confirmation of a cAMP-independent pathway was obtained when DA inhibited TSH-stimulated cAMP formation, but, contrary to T₄ release, this inhibition was not reversed by dopaminergic or adrenergic blockers. Presumably, therefore, DA inhibition of TSH-stimulated cAMP production was not related to T₄ release.

We conclude that 1) DA inhibits TSH-stimulated T₄ release in mouse thyroids via a-adrenergic and dopaminergic receptors; 2) L-DOPA has to be converted to DA to produce inhibition; and 3) cAMP is unlikely to be an intermediary in DA inhibition. (Endocrinology 118: 632–636, 1986)

Footnotes

^* This work was supported in part by V.A. funds.

Received May 22, 1985.

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