Growth hormone secretion in response to the new centrally acting antihypertensive agent moxonidine in normal human subjects: comparison to clonidine and GHRH

Summary

It is well established that the central α₂-adrenergic agonist Clonidine can enhance growth hormone (GH) secretion in humans. This effect is most likely due to stimulation of hypothalamic growth hormone releasing hormone (GHRH) release. To determine the potency of the new I₁-imidazoline receptor agonist moxonidine to release pituitary hormones, 12 normal volunteers received clonidine (0.3 mg), moxonidine (0.3 mg), or placebo orally according to a randomized, double-blind protocol. Blood was drawn prior and up to 180 min after drug administration for determination of GH, adrenocorticotropic hormone (ACTH), prolactin, thyrotropin (TSH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), glucose, Clonidine, and moxonidine concentrations. The results were compared to those obtained in a standard GHRH stimulation test (1 µg/kg i.v.).

Serum GH levels increased significantly in response to GHRH, clonidine, and moxonidine. However, the increase was less pronounced 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 observed in the concentration of any other pituitary hormone.

We conclude that the new I₁-imidazoline receptor agonist moxonidine stimulates GH release to a similar extent as Clonidine.

Key words

Alpha 2-receptor agonist - Clonidine - imidazoline receptor - growth hormone - growth hormone releasing hormone