Noradrenergic Modulation of Human Pancreatic Growth Hormone-Releasing Factor (hpGHRFl-44)-Induced Growth Hormone Release in Conscious Male Rabbits: Involvement of Endogenous Somatostatin*

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Abstract
To clarify the role of noradrenergic neurons in the regulation of GH [growth hormone] secretion, the effects of i.v. administered noradrenergic antagonists were investigated in freely moving, conscious male rabbits. During a 6 h observation period (1030-1630 h), control rabbits manifested pulsatile GH secretion with surges between 1030-1200 and 1415-1630 h. Phenoxybenzamine, (POB), an .alpha.-adrenergic blocker (5 mg/kg, twice), abolished the episodic GH surges; propranolol, a .beta.-adrenergic blocker (2.5 mg/kg, twice), did not. The bolus injection (1 or 10 .mu.g) of synthetic human pancreatic GH-releasing factor (hpGHRF) with 44 amino acid residues (hpGHRF1-44) resulted in significant rises in the plasma GH of control animals. The plasma GH responses to hpGHRF1-44 were significantly larger in propranolol-treated than control rabbits. In contrast, POB completely suppressed the hpGHRF1-44-induced GH release. The injection of antisomatostatin (SRIF) serum into POB-treated rabbits did not yield a disinhibition of the episodic GH surges but restored the plasma GH rises after hpGHRF1-44 injection. Noradrenaline [norepinephrine] plays an important role in regulating GH secretion in the rabbit. .alpha.-Noradrenergic blockade evidently suppresses GH release not only by inhibiting the release of hypothalamic GHRF but also by stimulating the secretion of SRIF and .beta.-noradrenergic blockade enhances GH release by inhibiting the release of SRIF from the hypothalamus.