Pharmacological evidence for opioid and adrenergic mechanisms controlling growth hormone, prolactin, pancreatic polypeptide, and catecholamine levels in humans.

A group of 14 healthy subjects received 50 mg/kg body weight of 2 deoxy-D-glucose (2DG) IV in a 20-minute infusion to induce glucoprivation and stimulate the release of growth hormone (GH), prolactin (PRL), pancreatic polypeptide (hPP), and catecholamines. Six subjects having spontaneously high GH baseline levels (greater than 8 ng/mL) failed to mount a GH response to 2DG-induced glucoprivation while eight subjects having low GH baseline levels (less than 8 ng/mL) all had increases (greater than 10 ng/mL) of GH levels after 2DG (P less than 0.05). Baseline level of GH was a reliable predictor of subsequent GH response to 2DG. Administration of the alpha 2-adrenoreceptor agonist clonidine (0.5 mg po) reliably increased GH levels (P less than 0.05). Elevated GH levels following clonidine administration abolished GH responses to subsequently infused 2DG (P less than 0.05). While these data do not exclude the possibility of a short loop feedback control of GH secretion, they strongly suggest that the direction of the GH response to a provocative stimulus is determined by the antecedent GH level and that an alpha-adrenoreceptor mechanism is involved in such a biphasic modulation of GH levels. Clonidine administration significantly reduced total catecholamine, pancreatic polypeptide, and prolactin response to 2DG while opiate receptor blockade with naloxone (10 mg IV bolus followed by 2 mg/hr) did not affect catecholamine and pancreatic polypeptide response but did slightly attenuate the GH and PRL response to glucoprivation. We conclude that alpha adrenoreceptor mechanisms are of major importance while opiate receptor mechanisms are of relatively minor importance in modulating the effects of glucoprivation on sympathetic outflow and hPP, GH, and PRL levels.