Acetylcholine and Norepinephrine: Compared Actions on Thyroid Metabolism

Acetylcholine (ACh; 5 × 10^-4 M), like norepinephrine (NE; 6 × 10^-6 M), as shown previously, stimulated iodide organification by mouse thyroids in vitro, while at the same time it inhibited TSH- or (Bu)₂cAMP-induced T₄ release. However, thyroid cAMP was not changed by ACh, suggesting that ACh, like NE, exerted its effects at a step beyond cAMP production. Also, while ACh increased cGMP concentrations, (Bu)₂cGMP and 8-bromo-cGMP were not effective on thyroid function in this system. Neurotransmitters, then, presumably do not exert their action through cyclic nucleotide stimulation. ACh-induced stimulation of organification and inhibition of release was reversed by 10^-5 M atropine (ATR) but not by 10^-5 M d-tubocurarine, indicating that muscarinic receptors were involved. ATR also reversed inhibition of T₄ release induced by NE, suggesting that the presynaptic cholinergic pathway may be responsible for stimulation of postsynaptic cholinergic and adrenergic neurotransmitters in the thyroid gland.