Abstract
Publisher Summary This chapter discusses the sympathetic regulation of thyroid hormone secretion. The finding of sympathetic nerve terminals very close to thyroid follicle cells signifies that there is a morphologic basis for a direct, nonvascular, influence of sympathetic stimuli on thyroid hormone secretion. There is also evidence that such an influence is exerted. In mice, whose TSH secretion has been eliminated, sympathetic stimulation or administration of norepinephrine (NE) or other arylmethylamines induces secretion of thyroid hormone, as reflected by signs of endocytosis of thyroglobulin followed by release of thyroidal radioiodine into the blood. The secretory response to sympathetic stimulation is restricted to the thyroid regions supplied by the stimulated nerve, indicating that the effect results from an action of NE released within the gland. The thyroid activation is probably induced by the amine as such the effect is augmented after pretreatment with a monoamine oxidase inhibitor, and the catecholamine precursor DOPA exerts a thyroid-stimulating effect only after its decarboxylation to dopamine. It is found that although catecholamines certainly affect thyroid blood flow, their stimulatory effect on the thyroid hormone secretion cannot entirely be explained by their influence on thyroid vessels, and it is rather the result of a direct action on the follicle cells.
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