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Piperidine Enhances Sleep-Related and Insulin-Induced Growth Hormone Secretion: Further Evidence for a Cholinergic Secretory Mechanism^*

Laboratory of Clinical Psychopharmacology, SMR, IRP, National Institute of Mental Health, Saint Elizabeth's Hospital Washington D.C. 20032 Unit on Sleep Studies, Biological Psychiatry Branch, DCBR, IRP, National Institute of Mental Health, NIH Bethesda, Maryland 20205
the Clinical Research Center, Department of Medicine, University of Rochester School of Medicine Rochester, New York 14642

Address all correspondence and requests for reprints to: W. B. Mendelson, M. D., Building 10, Room 3N224, National Institutes of Health, Bethesda, Maryland 20205.

Piperidine, a nicotinic cholinergic receptor stimulator, was used in paired design studies of sleep-related and insulin-induced GH and PRL secretion. For the sleep studies, 100 mg piperidine or an equal volume of saline were infused for 30 min starting at sleep onset in eight normal volunteers. The same dose of piperidine was infused for 30 min (beginning 15 min before insulin injection) in an additional eight volunteers undergoing insulin tolerance tests. After piperidine administration, there was a significant (P < 0.01) enhancement of sleep-related GH secretion, but no change in PRL. GH concentrations during the first 2 h of sleep were 7.2 ± 1.2 ng/ml after saline and 15.2 ± 2.9 ng/ml after piperidine (P < 0.01). No alteration n i any measured sleep parameter was noted with the drug. Piperidine did not affect the daytime insulin-induced secretion of either GH or PRL, as assessed by an analysis of variance.However, paired analysis of increments and areas under the response curves indicated a statistically significant effect for GH but not PRL. The maximum GH increment with piperidine was 48.0 ± 4.3 ng/ml, compared to 36.8 ± 3.6 ng/ml with saline (P < 0.01). Piperidine given alone did not influence daytime concentrations of GH. These data are consistent with the view proposed by us, on the basis of methscopolamine inhibition of nocturnal GH secretion, that cholinergic pathways play a facilitatory role in sleep-related and insulin-induced GH secretion. Thus, cholinergic mechanisms stimulate GH secretion. Nicotinic as well as muscarinic pathways appear to be involved, although the quantitative nicotinic contribution seems to be smaller than that associated with muscarinic sites.

^* This work was supported in part by Research Grant RR-00044 from the Division of Research Resources, NIH.

Received January 23, 1980.

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