| 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 that beta 2-adrenergic receptors mediated this phasic GH release, while having no apparent effect on 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 microM l-norepinephrine (n = 4). Direct binding studies in membrane particulates of rat AP confirmed receptors of the beta 2-subtype. Iodocyanopindolol 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. |
