Thyroid hormone and norepinephrine: effects on alpha-2, beta, and reuptake sites in cerebral cortex and heart

Abstract

Thyroid hormone produces metabolic effects similar to those of stimulation of noradrenergic receptors. It has been reported, however, that norepinephrine turnover is reduced during thyrotoxicosis and that beta-noradrenergic receptor number is increased. Metabolic effects of thyroid hormone may therefore reduce noradrenergic activity. We examined effects of thyroid hormone administration or production of hypothyroidism with methimazole on receptors associated with regulation of noradrenergic function. Treatment with thyroid hormone increased beta-receptor binding, increased alpha-2 receptor binding, and decreased desipramine binding, opposite to effects of hypothyroidism produced by methimazole. Heart was more sensitive than brain to these effects. These data are consistent with reduced noradrenergic activity during hyperthyroidism, possibly mediated by an increase in autoreceptor function.