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,
COVADONGA MURUAIS and
CARLOS DIEGUEZ
Departments of Physiology (CM., CD.) and Medicine (F.F.C, B.B.), Hospital General Galicia, Santiago de Compostela Spain
The Endocrine Section, Faculty of Medicine, Santiago University, Santiago de Compostela Spain
Address all correspondence and requests for reprints to: F. F. Casanueva, M.D., P.O. Box 563, Santiago de Compostela, Spain.
It is widely accepted that chronic administration of corticoids in man inhibits the GH response to all of the stimuli tested so far. To study the action of corticoids administered acutely, several dexamethasone challenge tests were performed, after which GH levels were measured for 7 h.
In eight volunteers, administration of 4 mg dexamethasone (Dex), iv, induced a clear-cut GH release compared with saline administration. The secretion followed an unusual pattern; basal GH levels (1.5 ± 0.1 µg/L) started rising 2 h after Dex injection, reaching a peak of 17.5 ± 4.4 µg/L after 3 or 3.5 h. Peak levels were maintained until 5 h post-Dex and decreased thereafter. Similar data were obtained when Dex was administered to five volunteers at the dose of 8 mg, orally, with a 30-min delay of the GH peak (19.6 ± 7.9 µg/L).
To study whether there was a cholinergic input responsible for the Dex action, another group of eight volunteers underwent three Dex tests (4 mg, iv) on three occasions, followed 90 min later by the administration of placebo (control), atropine (0.5 mg, iv), or pyridostigmine (120 mg, orally). The Dex-induced GH peak (20.8 ± 5.2 µg/L) was not significantly increased by pyridostigmine (cholinergic agonist) treatment (24.2 ± 4.0 µg/L). The blockade of muscarinic receptors by atropine induced a delay in the Dex-induced secretory peak, which appeared at 5 h. However, the Dex-atropine GH peak (14.9 ± 4.1 µg/L) was not different from the Dex-placebo one.
In conclusion, Dex alone is able to induce a clear-cut GH secretion in man. The stimulus followed a peculiar time pattern, with peaks levels attained 3 h after either iv or oral administration.
* This work was supported by Grants FIS88 88-0818 and 89-0766 and Xunta de Galìcià.
Recipient of a research fellowship from the Fondo de Investig
ciònes Sanitarias SS, Spanish Ministry of Health.
Received March 27, 1989.
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