β-Adrenergic Binding and Secretory Responses of the Anterior Pituitary*

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Abstract
Our studies demonstrated that .beta.-adrenergic agonists stimulate the release of GH from rat anterior pituitary (AP) cells in vitro. Concentration-response experiments with .beta.-adrenergic agonists demonstrated tht .beta.2-adrenergic receptors mediated this phasic GH release, while having no apparent effect of PRL or LH release. The ACTH response to .beta.-adrenergic agonists was equivocal. Half-maximal stimulation of GH release occurred at 14 .+-. 2 (.+-. SE) nM isoproterenol. 160 .+-. 30 nM epinephrine, and over 1 .mu.M l-norepinephrine (n = 4). Direct binding studies in membrane particulates of rat AP confirmed receptors of the .beta.2-subtype. Iodocyanopinodolol binding to .beta.-adrenergic receptors of rat AP yielded a dissociation constant of 4.6 .+-. 0.1 pM and a maximal capacity of 1.9 .+-. 0.4 fmol/mg protein (n = 3). In contrast, porcine AP contained .beta.1-adrenergic receptors. These results support the hypothesis that the endogenous .beta.2-adrenergic agonist l-epinephrine may be a GH-releasing factor of physiological significance in the rat.
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