Direct Adrenergic Stimulation of the Release of Thyrotropin and Its Subunits from the Thyrotropein Vitro*

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Abstract
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 < 0.001, P < 0.001, and P < 0.01, respectively). E, norepinephrine, and phenylephrine, all .alpha.-adrenergic agonists, caused significant increases in TSH release, with half-maximal effects at 4.3 .times. 10-7, 6.8 .times. 10-7, and 8.2 .times. 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 .times. 10-7 M) with a submaximal concentration of phenylephrine (5 .times. 10-7 M) caused a rise in TSH release greater (P < 0.02) than that seen with P alone. The .alpha.-adrenergic antagonists phentolamine and fluphenazine completely inhibited (P < 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.