Acute Administration of Corticoids: A New and Peculiar Stimulus of Growth Hormone Secretion in Man*

Abstract

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 micrograms/L) started rising 2 h after Dex injection, reaching a peak of 17.5 +/- 4.4 micrograms/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 micrograms/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 micrograms/L) was not significantly increased by pyridostigmine (cholinergic agonist) treatment (24.2 +/- 4.0 micrograms/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 micrograms/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.

Opposing influences of glucocorticoids and interleukin‐1β on the secretion of growth hormone and ACTH in the rat in vivo: role of hypothalamic annexin 1

“…The positive e ect of the exogenous corticosterone on the secretion of GH reported here accords with data from a number of clinical studies which have demonstrated prompt increases in serum GH following acute administration of glucocorticoids by mouth or parenterally (Buguera et al, 1990;Casanueva et al, 1990;Muruais et al, 1991;Pineda et al, 1994;Pinto et al, 1997;Pellini et al, 1998) and advocated a role for GCs in the diagnosis of GH de®ciency (Pineda et al, 1994;Pellini et al, 1998). Our ®nding that the hypersecretion of GH provoked by a single injection of corticosterone in the rat is (a) blocked speci®cally by central but not peripheral administration of anti-annexin 1 pAb and (b) mimicked by a central injection of annexin 1 Ac2 ± 26 suggests that the steroid exerts its positive in¯uence on the GH axis via an annexin 1-dependent mechanism within the hypothalamus.…”

“…This is due largely to actions of the steroids at the hypothalamic level which increase the expression and release of somatostatin (Papachristou et al, 1994;Fife et al, 1996;Lam & Srivastava, 1997) and decrease the production of GH releasing hormone (GHRH, Fernandez-Vazquez et al, 1995;Fife et al, 1996;Lam & Srivastava, 1997). Paradoxically, the impact of the consequent change in the hypothalamic drive to the somatotrophs is attenuated by concomitant actions of the steroids at the pituitary level which increase GHRH receptor (Tamaki et al, 1996;Miller & Mayo, 1997) and GH (Oosterom et al, 1983;Evans et al, 1992;Nogami et al,complicated by ®ndings in man that acute administration of GCs causes a transient (3 ± 4 h), but marked, increase in serum GH (Buguera et al, 1990;Casanueva et al, 1990;Muruais et al, 1991;Pineda et al, 1994;Pinto et al, 1997;Pellini et al, 1998). The mechanism by which the GCs evoke this secretory response is unclear.…”

“…The mechanism by which the GCs evoke this secretory response is unclear. Casanueva et al (1990) argued against an action at the pituitary level, a view which is supported by observations that, in stark contrast to their longer term actions, GCs inhibit GHRH-induced GH release from rodent pituitary tissue in vitro within this short timeframe (Vale et al, 1983;Ceda et al, 1987;Taylor et al, 2000a). Other data favour a transient action at the hypothalamic level which augments GHRH release (Fernandez-Vazquez et al, 1995) and/or depresses the secretion of somatostatin (Muruais et al, 1991).…”

Organization and Integration of the Endocrine System: The Arousal and Sleep Perspective

“…Acute elevations of GH concentration in plasma may occur at the onset of the stress response, however, or after acute administration of glucocorticoids, presumably through stimulation of the GH gene by glucocorticoids through glucocorticoid-responsive elements in its promoter region. [82] In addition to the direct effects of glucocorticoids, which are pivotal in the suppression of growth observed in prolonged stress, increases in somatostatin secretion caused by CRH, with resultant inhibition of GH secretion, have been implicated as a potential mechanism of stress-related suppression of GH secretion. [83] In several stress system-related mood disorders with a hyperactive HPA axis, such as anxiety or melancholic depression, levels of GH or insulin-like growth factor-1 (IGF-1), or both, are significantly decreased.…”

Na+, K+-ATPase content in skeletal muscle of dogs with pituitary-dependent hyperadrenocorticism

“…First, long-term exposure to glucocorticoids, as investigated in our study, may have different effects on Na + , K + -ATPase content than relatively short-term exposure. Similarly, GH secretion is acutely stimulated by administration of glucocorticoids such as dexamethasone [27,28]. However, long-term cortisol treatment suppresses GH secretion through increased somatostatin tone [29].…”