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

In conscious, chronically cannulated, unrestrained rats, systemic administration of catecholamines increases the plasma levels of beta-endorphin-like immunoreactivity (beta Ei). In euthyroid rats, this effect is mediated by both alpha 1 and beta-adrenergic 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 either phenylephrine or isoproterenol, suggesting that both agents act directly on the pituitary. Hypothyroidism induced by surgical 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 micrograms/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.