GROWTH-HORMONE SECRETION IN RESPONSE TO THE NEW CENTRALLY ACTING ANTIHYPERTENSIVE AGENT MOXONIDINE IN NORMAL HUMAN-SUBJECTS - COMPARISON TOCLONIDINE AND GHRH

It is well established that the central alpha(2)-adrenergic agonist cl onidine can enhance growth hormone (GH) secretion in humans. This effe ct is most likely due to stimulation of hypothalamic growth hormone re leasing hormone (GHRH) release. To determine the potency of the new I- 1-imidazoline receptor agonist moxonidine to release pituitary hormone s, 12 normal volunteers received clonidine (0.3 mg), moxonidine (0.3 m g), or placebo orally according to a randomized, double-blind protocol . Blood was drawn prior and up to 180 min after drug administration fo r determination of GH, adrenocorticotropic hormone (ACTH), prolactin, thyrotropin (TSH), luteinizing hormone (LH), follicle-stimulating horm one (FSH), glucose, clonidine, and moxonidine concentrations. The resu lts were compared to those obtained in a standard GHRH stimulation tes t (1 mu g/kg i.v.). Serum GH levels increased significantly in respons e to GHRH, clonidine, and moxonidine. However, the increase was less p ronounced in response to clonidine and moxonidine as compared to GHRH (mean +/- SEM): after clonidine, GH increased from 0.2 +/- 0.1 to 5.4 +/- 1.5 ng/ml, p < 0.05; moxonidine incrased GH levels from 0.1 +/- 0. 04 to 4.8 +/- 1.9 ng/ml (p < 0.05); GHRH caused an increase from 0.01 +/- 0.05 to 14.8 +/- 2.5 ng/ml p < 0.05). No significant change was ob served in the concentration of any other pituitary hormone. We conclud e that the new I-1-imidazoline receptor agonist moxonidine stimulates GH release to a similar extent as clonidine.