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Many of the signs and symptoms characteristic of the hyperthyroid state can be elicited in closely similar form by the administration of epinephrine or norepinephrine. Both in clinical and in experimental hyperthyroidism, some receptor systems are known to be more sensitive to catecholamines than they are in the euthyroid state (1). It has been frequently suggested, therefore, that the manifestations of hyperthyroidism are to some extent indirect effects, secondary to enhancement of effective sympathetic activity, rather than direct effects of the thyroid hormone itself. There is convincing evidence that at least some of the
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Eaton et al. (1965) studied this question.
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