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Suppression of the Growth Hormone (GH) Response to Clonidine and GH-Releasing Hormone by Exogenous GH^*

Department of Pediatrics Yale University School of Medicine New Haven, Connecticut 06510
Stanford University School of Medicine Stanford, California 94305

Address all correspondence and requests for reprints to: Joseph M. Gertner, M.B., M.R.C.P., Department of Pediatrics, The New York Hospital-Cornell medical Center, 525, East 68th Street, New York, New York 10021.

GH release in response to clonidine and human GH-releasing hormone-(1–44)(hGHRH-44) was assessed in 11 boys (aged 7–14 yr) with short stature, who had normal GH secretion. The response to these 2 provocative stimuli was repeated after, respectively, 2 and 3 days of treatment with human GH (0.1 U/kg, im). Exogenous GH significantly blunted the response to both clonidine [the mean 2-h integrated serum GH concentration falling from 1050 ± 350 (±SEM) to 749 ±297 ng/ml·min; P = 0.03] and hGHRH-44, the 2-h integrated GH concentration falling from 1553 ± 358 to 547 ±202 ng/ml · min; (P = 0.03). Plasma insulin-like growth factor (IGF-II) concentrations did not change after GH administration. In contrast, plasma IGF-I (somatomedin-C) concentrations increasedfrom 97 ±16 ng/ml before administration of GH to 142 ± 32 ng/ml (P = 0.05) after two days and 149± 23 ng/ml (P < 0.01) after the third treatment day. However, no correlation was found between thechanges in response to clonidine or hGHRH-44 and changes in circulating levels of IGFI.

Our data confirm the existence of GH-dependent feedback inhibition of GH release during childhood and suggest that this inhibition operates, at least in part, at the level of the pituitary. While participation of the IGFs/somatomedins in this feedback loop cannot be excluded, the inhibitoryeffects of exogenous GH do not depend directly on circulating plasma IGF-I or IGF-II levels.

^* Presented in part at the May 1985 Meeting of the Society for Pediatric Research/American Pediatric Association, Washington D.C. This work was supported by NIH Grant RR-00125 to the Yale Children's Clinical Research Center.

Received August 9, 1985.

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