Our studies demonstrated that β-adrenergic agonists stimulate the release of GH from rat anterior pituitary (AP) cells in vitro. Concentration-response experiments with β- adrenergic agonists demonstrated that β2-adrenergic receptors mediated this phasic GH release, while having no apparent effect on PRL or LH release. The ACTH response to β-adrenergic agonists was equivocal. Half-maximal stimulation of GH release occurred at 14 ± 2 (±SE) nM isoproterenol, 160 ± 30 nM epinephrine, and over 1 μM l-norepinephrine (n = 4). Direct binding studies in membrane particulates of rat AP confirmed receptors of the β2-subtype. Iodocyanopindolol binding to β-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 β1-adrenergic receptors. These results support the hypothesis that the endogenous fcadrenergic agonist l-epinephrine may be a GH-releasing factor of physiological significance in the rat.
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