Adrenergic Regulation of β-Endorphin Secretion from Anterior Pituitary in Conscious Rats: Effects of Thyroid State

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Abstract
In conscious, chronically cannulated, unrestrained rats, systemic administration of catecholamines increases the plasma levels of .beta.-endorphin-like imunoreactivity (.beta.Ei). In euthyroid rats, this effect is mediated by both .alpha.1 and .beta.-adrenertic receptors; the rise in plasma .beta.Ei caused by isoproterenol is blocked by 1 mg/kg propranolol, and the similar effects of norepinephrine and phenylephrine are blocked by 0.1 mg/kg prazosin. Both types of responses are completely suppressed by a 4-h pretreatment of rats with 0.1 mg/kg dexamethasone, indicating the anterior pituitary origin of the .beta.Ei released. Prior sectioning of the pituitary stalk does not significantly reduce the response to other phenylephrine or isoproterenol, suggesting that both agents act directly on the pituitary. Hypothyroidism induced by thyroidectomy does not influence the .beta.Ei response to isoproterenol, which remains sensitive to block by propranolol or suppression by dexamethasone. However, neither norepinephrine nor phenylephrine is able to increase plasma .beta.Ei in the hypothyroid animals. Both isoproterenol and phenylephrine remain fully effective in rats made hyperthyroid by daily injections of 40 .mu.g/kg T3 for 4 days. We propose that in unstressed rats catecholamines increase plasma .beta.Ei by a direct action on the anterior pituitary via either .alpha.1- or .beta.-adrenergic receptors, and that expression of the .alpha.1-, but not the .beta.-adrenergic response is regulated by thyroid hormones.
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