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Enhancement of Cholinergic Tone by Pyridostigmine Promotes Both Basal and Growth Hormone (GH)-Releasing Hormone-Induced GH Secretion in Children of Short Stature^*

Department of Biomedical Endocrinology and Metabolism and Gastroenterology and Clinical Pediatrics 2, University of Turin Turin
The Department of Pharmacology, University of Milan Milan, Italy

Address all correspondence and requests for reprints to: Dr. Ezio Ghigo, Divisione di Endocrinologia, Ospedale Molinette, Corso Polonia 14,10126 Torino, Italy.

Increased cholinergic tone induced by pyridos-tigmine (PD) increases basal plasma GH levels and potentiates the GH response to GHRH in normal adults. In this study the effects of PD (60 mg, orally) on both basal and GHRH (1 µg/kg)-induced GH secretion in seven children with familial short stature (FSS), six with GH deficiency (GHD) and 10 with constitutional growth delay (CGD) were studied and compared with results obtained by stimulation with insulin-induced hypoglycemia (IH) and GHRH alone. The mean peak plasma GH levels were variable, but individual values were frequently low in all groups after both IH [FSS, 9.7 ± 1.3 (±SEM) ng/mL; GHD, 1.6 ± 0.4 ng/mL; CGD, 7.0 ± 0.8 ng/mL] and GHRH (FSS, 23.8 ± 6.6 ng/mL; GHD, 11.1 ± 5.8 ng/mL; CGD, 15.1 ± 4.5 ng/mL) administration. PD induced GH responses (FSS, 14.5 ± 1.6 ng/mL; GHD, 3.8 ± 0.8 ng/mL; CGD, 18.3 ± 3.2 ng/mL) that in many children in the FSS and CGD groups were higher than those after IH and GHRH treatment. PD clearly increased the GH response to GHRH in all children [FSS, 69.5 ± 9.4 ng/mL (P < 0.01 vs. other stimuli); GHD, 18.0 ± 7.5 ng/mL; CGD, 50.0 ± 8.5 ng/mL (P < 0.01 vs. other stimuli)]. We conclude that in children with short stature, as in adults, enhancement of cholin-ergic tone increases both basal and GHRH-induced GH secretion, and that PD plus GHRH is the best provocative stimulus for evaluating the somatotroph response.

^* This work was partially supported by a grant from the Ministero della Pubblica Istruzione. These data have been partially presented at the Second Meeting of the European Neuroendocrine Association, Milan, Italy, 1985, and at the First International Congress of Neuroen-docrinology, San Francisco, CA, 1986.

Received November 24, 1986.

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