Failure of pyridostigmine to increase both basal and GHRH-induced GH secretion in the night.

The aim of this study was to verify that the stimulatory effect of cholinergic agonists on both basal and stimulated GH release observed in the morning persists in the night. The effects of pyridostigmine (120 mg orally), a cholinesterase inhibitor, on both basal and GHRH (1 micrograms/kg iv)-induced GH secretion were studied in 8 healthy volunteers, aged 22-30 years. In the morning, administration of pyridostigmine induced a significant increase in basal GH levels compared with saline (area under the response curve, mean +/- SEM: 277.0 +/- 54.0 vs 49.7 +/- 8.2 micrograms.l-1.h-1, p less than 0.02) as well as a strong potentiation of the GHRH-induced GH release (2117.6 +/- 353.0 vs 427.9 +/- 87.0 micrograms.l-h-1, p less than 0.02). In the night, GH secretion after pyridostigmine did not differ from saline (194.5 +/- 21.9 vs 89.4 +/- 28.7 micrograms.l-1.h-1). Moreover pyridostigmine failed to potentiate the GHRH-induced GH increase (1071.9 +/- 170.4 vs 740.2 +/- 150.9 micrograms.l-1.h-1). The pyridostigmine + GHRH-induced GH rise during the night was lower (p less than 0.05) than in the morning. All together, these data seem to indicate that cholinergic neurons controlling GH secretion are already maximally stimulated at night. As cholinergic activity negatively modulates SRIH secretion, our findings suggest that a reduced somatostatinergic tone in the hypothalamus is present during the night.