Regulation of Thyrotropin Secretion by the Central Epinephrine System

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Abstract
In the present investigation CNS epinephrine (EPI) biosynthesis was selectively interrupted with specific norepinephrine N-methyltransferase (NMT) inhibitors, SK&F 64139 (Smith, Kline and French Laboratories) and LY 78335 (Eli LIlly and Co. Research Laboratories), to determine the effects of central EPI depletion on basal and cold, thyrotropin-releasing hormone, and hypothalamic somatostatin antiserum induced thyrotropin (TSH) secretion in chronically cannulated rats. Because these NMT inhibitors also are .alpha.2-adrenergic receptor blockers, the effects of .alpha.2- and .alpha.1-adrenergic blockade and .alpha.2-activation on plasma TSH were assessed with rauwolscine and corynanthine and B-HT 933, respectively. Serum T4 and plasma corticosterone were also measured. Blockade of CNS EPI synthesis resulted in inhibition of basal and cold were thyrotropin-releasing hormone induced TSH release, suppression of serum T4, and increased corticosterone release. The stimulatory effect of SRIF antiserum on plasma TSH was not altered by SK&F 64139, .alpha.2-adrenergic blockade suppressed plasma TSH levels, but not to the same degree as the NMT inhibitors; activation of .alpha.2-receptors enhanced TSH secretion. Thus, it is possible that part of the effect of the NMT inhibitors on TSH was due to .alpha.2-blockade, .alpha.1-adrenergic blockade also lowered plasma TSH. These results indicate that (1) central EPI systems have a stimulatory role in TSH regulation, possibly mediated by .alpha.2-adrenergic receptors, (2) cold-induced TSH release is mediated, in part, by EPI, and (3) central EPI systems exert an inhibitory effect on the hypothalamic-pituitary-adrenal axis.

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