The study shows that activating alpha‑2 adrenergic receptors (with the drug clonidine) can boost the growth‑hormone‑releasing effect of GRF‑1‑29 in rats, but only when the brain's somatostatin (a hormone that blocks growth hormone) is naturally high. When somatostatin is already low, clonidine doesn’t make a difference. This suggests that alpha‑2 adrenergic activity can lift the brake that somatostatin puts on growth hormone release.

This study was undertaken to investigate whether or not alpha 2-adrenergic pathways would negatively modulate the hypothalamic somatostatin release in rats. To induce pharmacological changes in SS release, three groups of male Sprague-Dawley rats (n = 30/group) were separately anesthetized by ip administration of urethan (which increases SS tone; 1.2 g/kg), pentothal (which impairs SS release; 30 mg/kg), or ketamine (which does not affect spontaneous SS secretion; 40 mg/kg). Ten rats from each group were challenged with GRF (2 micrograms/kg iv), clonidine (40 micrograms/kg iv), or GRF plus clonidine. Administration of clonidine markedly increased the GH responsiveness to GRF in rats anesthetized with urethane or ketamine. In contrast, the GH response to GRF was not modified by clonidine in rats anesthetized with pentothal. These results show that alpha 2-adrenergic stimulation only modifies the GRF-induced GH rise when SS release is high. Therefore, in rats, central alpha 2-adrenergic pathways appear to play a main inhibitory effect on hypothalamic SS secretion.