Direct adrenergic stimulation of the release of thyrotropin and its subunits from the thyrotrope in vitro

• Published in: Endocrinology (Philadelphia) Vol. 113; no. 4; p. 1244
• Main Authors: Klibanski, A, Milbury, P E, Chin, W W, Ridgway, E C
• Format: Journal Article
• Language: English
• Published: United States 01-10-1983
• Subjects: Adrenergic alpha-Agonists - pharmacology; Adrenergic alpha-Antagonists - pharmacology; Adrenergic beta-Antagonists - pharmacology; Animals; Cattle; Cells, Cultured; Dose-Response Relationship, Drug; Glycoprotein Hormones, alpha Subunit; Male; Peptide Fragments - secretion; Pituitary Gland, Anterior - drug effects; Pituitary Gland, Anterior - secretion; Pituitary Hormones, Anterior - secretion; Thyrotropin - secretion; Thyrotropin-Releasing Hormone - pharmacology
• ISSN: 0013-7227
• DOI: 10.1210/endo-113-4-1244

Adrenergic effects on TSH and subunit secretion were investigated in bovine anterior pituitary monolayer cultures. Epinephrine (E) (10(-6) M) caused a significant increase in TSH, alpha-subunit, and TSH beta release into the medium (P less than 0.001, P less than 0.001, and P less than 0.01, respectively). E, norepinephrine, and phenylephrine, all alpha-adrenergic agonists, caused significant increases in TSH release, with half-maximal effects at 4.3 X 10(-7), 6.8 X 10(-7), and 8.2 X 10(-7) M, respectively. However, isoproterenol, a beta-adrenergic agonist (10(-7)-10(-4) M), did not alter TSH or subunit release. Clonidine, an alpha 2-adrenergic agonist (10(-7)-10(-4) M), had no effect on TSH or subunit secretion; however, coincubation of clonidine (5 X 10(-7) M) with a submaximal concentration of phenylephrine (5 X 10(-7) M) caused a rise in TSH release greater (P less than 0.02) than that seen with P alone. The alpha-adrenergic antagonists phentolamine and fluphenazine completely inhibited (P less than 0.001) the E-induced rise in TSH and subunits. In contrast, the beta-adrenergic antagonists propranolol and metoprolol did not significantly inhibit the stimulation of TSH by E. TSH and subunit secretion is stimulated by adrenergic agonists acting directly on the pituitary, and this is probably mediated via an alpha-adrenergic receptor.