Portal de Periódicos da CAPES

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

1984; Oxford University Press; Volume: 114; Issue: 4 Linguagem: Inglês

10.1210/endo-114-4-1402

1945-7170

Kazuo Chihara, Naoto Minamitani, Hidesuke Kaji, Hitoshi Kodama, Tetsuya Kita, Takuo Fujita,

Pancreatic function and diabetes

To clarify the role of noradrenergic neurons in the regulation of GH secretion, the effects of iv 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 α-adrenergic blocker (5 mg/kg, twice), abolished the episodic GH surges; propranolol, a β-adrenergic blocker (2.5 mg/kg, twice), did not. The bolus injection (1 or 10 μg) of synthetic human pancreatic GH-releasing factor (hpGHRF) with 44 amino acid residues (hpGHRFl-44) resulted in significant rises in the plasma GH of control animals. The plasma GH responses to hpGHRFl-44 were significantly larger in propranolol-treated than control rabbits. In contrast, POB completely suppressed the hpGHRFl-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 hpGHRFl-44 injection. These results indicate that noradrenalin plays an important role in regulating GH secretion in the rabbit. We propose that a-noradrenergic blockade suppresses GH release not only by inhibiting the release of hypothalamic GHRF but also by stimulating the secretion of SRIF and that β-noradrenergic blockade enhances GH release by inhibiting the release of SRIF from the hypothalamus. (Endocrinology114: 1402, 1984)