On the Mechanism of Growth Hormone Autofeedback Regulation: Possible Role of Somatostatin and Growth Hormone-Releasing Factor*

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Abstract
To determine the role of somatostatin (SRIF) and GH-releasing factor (GRF) in GH autofeedback, 20 μg rat GH in 2 μl were injected into the third ventricle (IVT) 1 or 3 h before injection of the α2-receptor stimulator clonidine (50 μg/kg, iv), which elevates plasma GH and TSH levels in normal rats. GH preinjected 1 or 3 h before clonidine significantly suppressed the clonidine-induced GH surge, whereas TSH release was not affected by GH. Preinjection of ovine LH IVT following the same protocol did not inhibit the clonidine-induced GH surge, suggesting a specific effect of IVT GH. Passive immunization with 400 μl sheep antisomatostatin serum did not reverse the inhibition of the clonidine-induced GH surge by exogenous GH administered IVT either 1 or 3 h before clonidine. The TSH response was augmented by this procedure. Furthermore, IVT GH did not reduce the surges of GH and TSH elicited by GRF (250 ng/kg, iv) and TRH (150 ng/kg, iv) administered 1 or 3 h after IVT rat GH. These results suggest that GH autofeedback is mediated by reduced GRF secretion, rather than enhanced SRIF release. (Endocrinology117: 2284–2292, 1985)