Adrenergic Regulation of β-Endorphin Secretion from Anterior Pituitary in Conscious Rats: Effects of Thyroid State
1987; Oxford University Press; Volume: 120; Issue: 3 Linguagem: Inglês
10.1210/endo-120-3-1073
ISSN1945-7170
AutoresEdward J.N. Ishac, Robert L. Eskay, Fusao Hirata, Julius Axelrod, George Kunos,
Tópico(s)Thyroid Disorders and Treatments
ResumoIn conscious, chronically cannulated, unrestrained rats, systemic administration of catecholamines increases the plasma levels of β-endorphin-like immunoreactivity (βEi). In euthyroid rats, this effect is mediated by both βi and β-adrenergic receptors; the rise in plasma βEi 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 j3Ei 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 βEi response to isoproterenol, which remains sensitive to block by propranolol or suppression by dexamethasone. However, neither norepinephrine nor phenylephrine is able to increase plasma βEi in the hypothyroid animals. Both isoproterenol and phenylephrine remain fully effective in rats made hyperthyroid by daily injections of 40 Mg/kg T3 for 4 days. We propose that in unstressed rats catecholamines increase plasma βEi by a direct action on the anterior pituitary via either α1 or β-adrenergic receptors, and that expression of the αi-, but not the β-adrenergic response is regulated by thyroid hormones. (Endocrinology120: 1073–1078, 1987)
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