0021-972X/91/7203-0675S03.00/0 Journal of Clinical Endocrinology and Metabolism Copyright © 1991 by The Endocrine Society

Vol. 72, No. 3 Printed in U.S.A.

Effects of Dexamethasone on Growth Hormone (GH)Releasing Hormone, Arginine- and Dopaminergic Stimulated GH Secretion, and Total Plasma Insulin-Like Growth Factor-I Concentrations in Normal Male Volunteers* JOHN P. MIELLt, ROGER CORDER$, FRANCOIS P. PRALONG, AND ROLF C. GAILLARD Neuroendocrine Unit, Department of Medicine, University Hospital of Geneva, 1211 Geneva 4, Switzerland

control, vs. 26.1 (15.1-38.6), DEX; P < 0.01; with an increase in AUC of 72%; P < 0.01]. In group B, under control conditions before glucocorticoid administration, the GH response to CV was significantly greater than that to dopamine in terms of both peak response [25.1 (8.6-30.9), CV, vs. 11.8 (5.5-16.4), dopamine; P < 0.05] and AUC [2406 ± 654 (CV) us. 658 ± 125 (dopamine); P < 0.01], suggesting that CV may be a useful adjunct in the diagnosis of GH deficiency. After DEX administration, responses to both dopaminergic agents were suppressed [CV, 6.7 (4.0-21.2); P < 0.01 vs. control response; and dopamine, 5.3 (4.87.9); P < 0.05 vs. control response]. When compared with the effects of dexamethasone on the GH response to arginine, the results with dopaminergic agents highlight important differences in the mechanisms of action of these indirectly acting GH secretagogues. Moreover, this may be of physiological importance, because in contrast to the inhibitory effect of glucocorticoid on GHRH-stimulated GH release, DEX treatment significantly increased basal plasma GH levels [1.4 (0.5-5.1) vs. control 0.3 (0.1-0.6) Mg/L; P < 0.001]. In addition, basal (0830 h) total plasma IGF-I levels measured after acid-ethanol extraction were significantly increased after DEX (417.0 ± 15.6; control, 300.1 ± 14.4 Mg/L; P < 0.001). (J Clin Endocrinol Metab 72: 675-681, 1991)

ABSTRACT. In man, glucocorticoid treatment and endogenous corticosteroid excess generally suppress stimulated GH release. However, such effects are not entirely consistent and depend on both the duration of pituitary exposure to steroids and the secretagogue employed. To further evaluate the effects of glucocorticoids in man, we have studied the response to four different GH stimulation tests before and after treatment with dexamethasone (DEX; 2 mg twice daily during 84 h). Twelve healthy male volunteers were divided into two groups of six subjects (groups A and B). Group A underwent stimulation tests with arginine (500 mg/kg, iv) and GH-releasing hormone (GHRH, 100 /ig, iv) before and after DEX treatment. Group B were subjected to stimulation tests with two dopaminergic agents, a novel nonergot D2-dopamine agonist CV205-502 (CV; 10 ng, iv) and dopamine (4 /ig/kg-min, iv), before and after DEX. Within each group, the effect of DEX on the different secretagogues was studied 4 weeks apart. GHRH-stimulated GH release was significantly blunted by DEX treatment [median peak GH value, 34.2 ng/h; 25-75th percentiles, 22.1-56.2), control, vs. 19.8 (9.7-34.5), DEX; P < 0.05; integrated GH secretion expressed as the area under the curve (AUC) was 48% lower after DEX; P < 0.01]. In the same group, DEX treatment significantly enhanced the response to arginine [10.6 (8.0-22.8),


LUCOCORTICOID excess undoubtedly inhibits somatic growth in man (1, 2) and laboratory animals (3, 4). Although the mechanism of this effect is probably unrelated to any action on pituitary GH release, it is frequently associated with attenuated GH responses to a number of pharmacological and physiological stimulants, including arginine (5), physical exercise (6), insulin-induced hypoglycemia (7-9), and GH-releasing Received August 9,1990. * This work was supported by Swiss National Research Foundation Grant 3.091.087. * Present address: Programmed Investigation Unit, Department of Medicine, King's College Hospital, Denmark Hill, London, SE5 8RX United Kingdom. * To whom all correspondence and requests for reprints should be addressed.

hormone (GHRH) (10). However, glucocorticoid suppression of GH secretion is not a constant finding; Nakagawa and colleagues (7) were unable to suppress the GH response to arginine in normal male volunteers, and Morris and colleagues (11) observed no differences between the GH responses to insulin-induced hypoglycemia in children receiving chronic high dose corticosteroids and age-matched asthmatic controls. Recently, permissive as well as suppressive effects of corticosteroids on stimulated GH release have been described, depending on the duration of pituitary exposure (12, 13). In vitro, glucocorticoids generally enhance both basal GH release (14, 15) and GHRH-stimulated GH release (16, 17), which at least in part is the consequence of an increase in GH gene transcription (18-20) and a gluco-


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corticoid-dependent increase in GHRH receptor density (21). Moreover, patients with idiopathic ACTH deficiency require adequate cortisone replacement to restore normal GH responses to stimulatory tests (22), indicating that a physiological level of corticosteroids is a prerequisite for the normal functioning of the hypothalamopituitary GH axis. Conversely, the observations that human GH administration cannot reverse the growth retardation associated with endogenous or exogenous hypercorticism (23, 24) suggests that glucocorticoid-induced changes in the hypothalamo-pituitary regulation of GH secretion are not the sole cause of growth failure; an equally important factor may be impairment of either the biosynthesis or peripheral actions of somatomedins (25). These various dichotomies have led us to study the effects of dexamethasone on stimulated GH secretion and total plasma insulin-like growth factor-I (IGF-I) levels in normal male volunteers. The secretagogues employed were GHRH, arginine, and two dopaminergic agents [dopamine and CV 205-502 (CV)]. The latter compound is a nonergot D2-dopamine agonist which we have recently shown to be a potent stimulator of GH release (26). To further evaluate the usefulness of CV as a GH secretagogue, the study has been designed to enable a direct comparison of its efficacy with that of dopamine. In addition, by determining the influence of glucocorticoids on the responses to GH stimulation with different secretagogues, we aimed to investigate whether arginine and dopaminergic agents have similar or different mechanisms of action. Materials and Methods Twelve male volunteers (mean weight, 68.3 ± 4 kg; age range, 21-25 yr) were studied after giving informed written consent. Six subjects were randomly assigned to study group A, and the remainder to group B. Subjects had no personal or family history of endocrine disorder, and were not on any form of medication. Each underwent biochemical, hematological, and clinical screening before inclusion in the study. All stimulation tests were carried out after an overnight fast with the subjects recumbent. Cannulae were placed in both antecubital fossae between 0700-0715 h, basal samples were taken at 0830 and 0859 h, and further blood samples were taken at the times indicated thereafter. Blood was immediately centrifuged, and plasma was stored at -20 C until assay. Group A: GHRH and Arginine The six volunteers tested with GHRH were administered 0.9% NaCl (100 mL) as an infusion between 0900-0930 h and received an iv bolus of GHRH (100 fig) at 0925 h. Blood samples were taken at 10-min intervals during the infusion, 5 min after injection of GHRH, and thereafter at 15-min intervals for 1 h and 30-min intervals for a further 2 h. The GHRH test was repeated after the supervised administration of eight 2-mg

JCE & M • 1991 Vol 72 • No 3

doses of dexamethasone (DEX) at 12-h intervals. The first dose was given the evening after the first test (2000 h), and the last dose at 0800 h on the morning of the second test. During this treatment period, blood was taken daily between 0800-0830 h for estimation of cortisol and total IGF-I. Four weeks later the same volunteers underwent testing with arginine (500 mg/kg in 200 mL Hartmann's solution) infused over 30 min (0900-0930 h). Samples were again taken at 10min intervals during the infusion, then at 15-min intervals for 1 h, and at 30-min intervals for a further 2 h. The arginine tests were repeated after the administration of DEX, as described above. Group B: Dopamine and CV Six volunteers were tested with CV (10 fig) infused in 10 mL saline over 30 min (0900-0930 h). Sampling times were identical to those during testing in group A, and the test was repeated after DEX treatment as described above. Four weeks later the same volunteers underwent testing with dopamine (4 jig/kg-min) infused in 10 mL saline over 30 min. Sampling times were identical, and the test was repeated after DEX treatment. All tests were carried out in a blind fashion. The protocol allowed us to compare the effects of four different stimulation tests before and after DEX treatment and also allowed a comparison of the effects of two dopaminergic secretagogues within the same group of volunteers. Assays Plasma GH was measured by immunoradiometric assay using reagents purchased from Nichols Institute (Allegro HGH, San Juan Capistrano, CA). This assay has a sensitivity of 0.02 Mg/L. Intra- and interassay coefficients of variation in our laboratory were 1.8% and 6.2%, respectively. IGF-I was measured by RIA, after ethanol-acid extraction of plasma samples, using a kit purchased from Nichols Institute. Intra- and interassay coefficients of variation were 2.4% and 5.8%, respectively. PRL was measured by immunoradiometric assay (Serono Diagnostic SA, Coinsins, Switzerland), with intra- and interassay variations of 2.3% and 5.7%, respectively. Plasma glucose was measured by the glucose oxidase methodology, and cortisol by a competitive protein binding assay method, as previously described (27), with intra- and interassay coefficients of variation of 5% and 10%, respectively (at 470 nmol/L). All samples from each subject undergoing a specific stimulation test before and after treatment with DEX were assayed simultaneously. Statistical Analyses Analysis of the GH results showed that the values did not have a normal distribution; therefore, GH levels at the various time points within each stimulation test were compared by Mann-Whitney U tests. However, for clarity, GH values are illustrated in Figs. 2 and 3 as the mean ± SEM. Because the peak values and maximum incremental rise over basal values were not always simultaneous, these variables were also calculated and compared by Mann-Whitney U test; for completeness their median values, 25-75th percentiles, and ranges are also

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EFFECTS OF DEX ON GH RELEASE shown (Table 2). Areas under the various stimulation curves (AUC) were calculated using a trapezoid method, and results are expressed in arbitrary units. Analysis of the AUCs, PRL, IGF-I, blood glucose, and cortisol concentrations revealed normal distributions, so these variables were compared by analysis of variance; when P < 0.05 the analysis was completed using Fisher's least significant difference test.

During each stimulation test, glucose was measured at hourly intervals and did not drop below 3.9 mmol/L, suggesting the absence of hypoglycemic stress effects. The mean 1200 h glucose concentration after dexamethasone treatment was significantly higher than that during the control stimulation test in all groups (5.53 ± 0.12; control, 4.87 ± 0.09; P < 0.001). The mean cortisol concentration before dexamethasone was 417.2 ± 30.7 nmol/L and demonstrated adequate suppression during the treatment period (51.1 ± 4.5, 12 h after 2 mg DEX; 39.9 ± 2.6, after the full course of DEX just before repeating the stimulation tests). Figure 1 shows individual basal GH values and total IGF-I values measured at 0830 h under control conditions and 4 days later after DEX treatment. Basal GH levels (micrograms per L) showed significant increases after DEX (control: median, 0.3; 25-75th percentile, 0.1-0.6; DEX: median, 1.4; 2575th percentile, 0.5-5.1; P < 0.001). Total IGF (micrograms per L) was measured at 0830 and 1200 h during the stimulation tests before and after DEX treatment and showed highly significant (P < 0.001) increases after

glucocorticoid (0830 h: control, 300.1 ± 14.4; DEX, 417.0 ± 15.6; 1200 h: control, 307.9 ± 13.3; DEX, 424.9 ± 16.4). The effects of the different stimulation tests on plasma PRL levels are shown in Table 1. After GHRH administration, no effect on PRL secretion was observed either during control conditions or after DEX. Arginine infusion induced a significant increase in PRL; this response was not significantly altered by DEX treatment. Intravenous administration of CV significantly suppressed PRL levels (basal, 8.6 ± 1.4 jug/L; 210 min postinfusion, 3.6 ± 0.8 iig/L, P < 0.01). Neither the basal levels nor the inhibitory effect of CV were significantly altered by DEX (basal, 7.2 ± 1.4 ^g/L; 210 min postinfusion, 2.5 ± 0.90 Mg/L; P < 0.01). DEX administration did not significantly alter the PRL response to dopamine infusion; the lowest levels on the 2 test days were recorded at 45 min, but these values were not significantly different from basal values on the respective days. Group A GH responses to an iv bolus of GHRH given at 0925 h are shown in Fig. 2a and Table 2. The peak GH values occurring 50 min after GHRH administration were re-

1 0 -»




o.i-i 700600-









FIG. 1. Upper panel, Basal plasma GH levels before (Pre) and after (Post) DEX treatment. Each point represents the mean of two basal estimations (0830 and 0859 h) for the 12 volunteers on the two separate occasions before control stimulation tests (n = 24) with the corresponding values 4 days later after DEX. Triangles represent the median values (A, pre-DEX; A, post-DEX). Bars indicate the 25th and 75th percentiles of each group of values. ***, P < 0.001. Lower panels Plasma total IGF-I levels at 0830 h before (Pre) and after (Post) treatment with DEX. Each point represents the IGF-I concentration for each of the 12 volunteers on 2 occasions as with GH (n = 24). Diamonds represent the means (•, pre-DEX; 0, post-DEX). Bars indicate the SEM. ***,P< 0.001.

TABLE 1. Basal and poststimulation PRL levels (micrograms per L) in the various study groups Basal

45 min

120 min

210 min


7.4 ± 0.7 5.9 ± 0.7

8.3 ± 1.0 6.5 ± 1.1

7.2 ± 1.4 6.3 ± 1.0

7.6 ± 1.3 6.2 ± 0.9

Arginine Arginine + DEX

7.1 ± 0.9 16.4 ± 1.9° 7.1 ± 0.8 6.6 ± 1.0 13.0 ± 2.66 7.0 ±1.0

6.3 ± 1.1 7.6 ± 0.9


8.6 ± 1.4 7.2 ± 1.4

5.8 ± 1.1 5.0 ± 1.2

Dopamine Dopamine + DEX

8.6 ± 1.2 5.9 ± 1.3

4.9 ± 0.6 8.0 ± 1.7 3.3 ± 0.5 6.5 ± 1.6


3.7 ±0.7" 3.6 ± 0.8° 3.4 ± 0.76 2.6 ± 0.9°

" P < 0.01 us. PRL levels on same day. h P < 0.05 vs. PRL levels on same day.

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9.2 ± 1.8 7.4 ± 1.5



•30 50i ^




incremental increases for each volunteer were not necessarily simultaneous, these were separately assessed, and median values are shown in Table 2 with their ranges and 25-75th percentiles. These results again demonstrate a significant attenuation of the GHRH-stimulated values by DEX, and the contrasting augmentation of arginine-induced GH responses after glucocorticoid administration.

90 120 150 180 210

Group B



w) 30



o 10



JCE&M-1991 Vol 72 • No 3




90 120 150 180 210

FIG. 2. a, GH responses to an iv bolus of 100 ng GHRH (arrow). • , Control; D, after DEX. Symbols represent the mean of six observations; bars indicate the SE. The shaded block corresponds to an infusion of 0.9% NaCl. *, P < 0.05; **, P < 0.01 (vs. DEX values), b, GH responses to arginine (500 mg/kg, iv) infused from 0-30 min (shaded area). • , control; 0, after DEX. Symbols represent the mean of six observations; bars indicate the SE. *,P< 0.05; **, P < 0.01 (vs. control values).

duced after DEX to approximately half the control response (P < 0.05). Similarly, after glucocorticoid treatment integrated GH secretion (AUC) over the 210-min sampling period was only 52% of that obtained during the control GHRH test (P < 0.05). With arginine the GH response was significantly potentiated by DEX treatment (Fig. 2b and Table 2); peak GH concentrations during stimulation were approximately 2.5-fold higher (P < 0.01), with the AUC also increased by 72% (P < 0.01). Because the individual peak values and maximum

The GH responses to CV (10 ng, iv) before and after treatment with glucocorticoid are shown in Fig. 3a and Table 2. After DEX the peak GH response to CV was inhibited by 70% (P < 0.01), and the integrated GH secretion (AUC) was reduced to 49% of the control response to CV (P < 0.05). With dopamine, similar results were observed (Fig. 3b). The peak GH response to dopamine was reduced by more than 50% after DEX (P < 0.05), but the mean AUC was not significantly altered (Table 2). Because the CV and dopamine stimulation tests were carried out on the same volunteers, a statistical comparison was performed of the efficacy of these two agents as GH secretagogues under control conditions before DEX administration (Table 2). CV was a more effective stimulator of GH in terms of each parameter illustrated (peak value, P < 0.05: maximum increment, P < 0.05; AUC, P < 0.01), with the peak values and AUC being approximately 2 and 3 times greater than those for dopamine, respectively.

Discussion In the adult human, long term glucocorticoid treatment has been found to suppress GH responses to most

TABLE 2. Comparison of the GH responses (micrograms per L) to stimulation tests with GHRH, arginine, CV, and dopamine, expressed as median values, 25-75th percentiles and ranges, with mean ± SEM for the areas under the various curves Peak GH (median)

25-75th percentile


AGH (median)

25-75th percentile




34.2 19.8"

22.1-56.2 9.7-34.5

16.9-66.5 5.2-37.0

33.3 17.6°

22.1-48.6 7.8-22.9

7.6-66.3 0-36.4

3961 ± 877 2060 ± 537*

Arginine Arginine + DEX

10.6 26.1"

8.0-22.8 15.1-38.6

3.9-27.8 8.0-43.9

6.6 21.1*

3.7-10.6 15.0-34.0

0-22.5 0-42.0

874 ± 250 1501 ± 227 6


25.1C 6.76

8.6-30.9 4.0-21.2

2.2-60.4 3.6-24.7

25.0c 5.4"

8.8-30.8 3.4-15.6

1.8-59.2 0.3-24.4

2406 ± 654 d 1169 ± 396°

Dopamine Dopamine + DEX

11.8 5.3°

5.5-16.4 4.8-7.9

5.4-16.6 3.3-9.2

11.4 3.2°

5.4-16.0 3.0-6.2

5.2-16.4 0-7.2

658 ± 125 463 ± 89


AGH, Maximal incremental GH rise over basal values. P < 0.05 us. response to the same stimulation test before DEX. b P< 0.01 vs. response to the same stimulation test before DEX. c P < 0.05 vs. dopamine stimulation before DEX. d P < 0.01 vs. dopamine stimulation before DEX. 0

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•30 50-




90 120 150 180 210




90 120 150 180 210





10 •30

FIG. 3. a, GH responses to CV (10 fig, iv) infused from 0-30 min (shaded area). • , Control; O after DEX. Symbols represent the mean of six observations; bars indicate the SEs. *, P < 0.05; **, P < 0.01 (vs. DEX values), b, GH responses to dopamine (4 ^g/kg-min) infused from 0-30 min (shaded area). A, Control; A, after DEX. Symbols represent the mean of six observations; bars indicate the SEs. *, P < 0.05 (us. DEX values).

secretagogues (5-10), yet this does not appear to be the case in children (11). The complexity of the interaction of glucocorticoids with GH secretion has been further emphasized by recent reports of short term DEX treatment enhancing responses to GHRH (12, 13) and other secretagogues (12). An initial permissive action on somatotrophs that increases sensitivity to GHRH and secretagogues evoking GHRH release would be in accordance with in vitro data demonstrating increased responsiveness after DEX treatment (14-17). This may then be followed by increased inhibitory central influences, particularly those mediated via higher somatostatinergic tone, leading to reduced responsiveness to stimulation (10, 28) and lower circulating GH levels (28). In contrast, enhanced responses to GHRH have been observed in male rats after DEX treatment (29). For this reason it has been argued that the rat is not a good model for the study of glucocorticoid-related effects on GH secretion (12). However, the underlying difference may simply reflect the higher frequency of GH secretion in male rats (30), during which somatostatin release is assumed to be low. Hence, if the permissive actions of glucocorticoids on somatotrophs are sustained, overriding suppressive effects may only be seen in conditions of naturally occurring high somatostatinergic tone, which may be the case in the adult human and the female rat (31), but not in the male rat (32) or, indeed, in children (11) where inhibitory effects are less apparent. This


theory is supported by observations in conscious male rats, in which treatment with DEX resulted in GH values being lower during trough periods (when naturally occurring somatostatin tone is high), yet the amplitude of peak values was increased (during periods of low somatostatin activity) compared with that in untreated controls (32). Furthermore, when GHRH activity in male rats was reduced by lesions of the arcuate nucleus, betamethasone treatment produced a reproducible reduction in GH levels (33), presumably because the effects of somatostatin were then unopposed. To further characterize the effects of glucocorticoid excess on GH release in man, we have compared their influence on responses to direct and indirect secretagogues. In this study we have recorded a small but consistent increase in plasma GH levels after 4 days of glucocorticoid administration. The significance of this change relative to actions at the pituitary and hypothalamic levels demonstrates that even in man an overriding increase in the influence of somatostatin after glucocorticoid administration is not necessarily present. However, in agreement with previous studies in man (10, 12, 13), we have demonstrated a significant reduction in GHRH-stimulated GH secretion after DEX treatment. The described effects of glucocorticoids on arginine induced GH secretion are less uniform, and heterogenous responses are often reported (7,12, 34). In this study one volunteer did not respond to arginine before DEX, but had an impressive response after treatment. Four of the remaining subjects also showed enhanced GH release after DEX, but one volunteer exhibited an attenuated GH response after glucocorticoid administration. These findings are compatible with suggestions that arginine acts through inhibition of somatostatin (35), hence allowing facilitatory effects of glucocorticoids on somatotroph cells to be expressed. However, the occurrence of poor responders to arginine under normal conditions and during glucocorticoid excess (Refs. 7, 12, and 34 and this study) indicates that not only is inhibition of somatostatin release required, but also the simultaneous presence of a stimulatory factor(s) is necessary for the full response to be manifested. Dopaminergic agents also stimulate the release of GH, although their mechanism(s) of action are not entirely clear. Dopamine does not cross the blood-brain barrier (36); thus, its effects are assumed to be at the level of the pituitary or median eminence. Furthermore, it has been claimed that some a-adrenergic activity cannot be excluded with the dose of dopamine used for such infusions (37). In contrast the D2-agonist, CV, has no aadrenergic activity and readily crosses the blood-brain barrier; hence, the two dopaminergic agents may elicit GH release via different mechanisms and/or sites of action. In particular, CV may have actions similar to

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those of dopamine outside the blood-brain barrier combined with additional central effects. This may account for CV being a significantly more potent secretagogue than dopamine. Nevertheless, the GH responses to both dopaminergic agents were reduced by DEX. As these effects of glucocorticoids were in direct contrast to those observed on arginine-induced GH secretion, it seems unlikely that dopaminergic agents and arginine share a common mechanism of action. Moreover, despite the similarities between the inhibition of dopaminergic and GHRH responses after DEX, dopaminergic agonists almost certainly act independently of GHRH, as the responses to a maximally stimulating dose of GHRH are increased by prior treatment with either dopamine (38) or bromocriptine (38, 39). As far as glucocorticoid inhibition of growth is concerned, changes in the hypothalamo-pituitary regulation of GH secretion are unlikely to account for this phenomenon, particularly when the lack of effect of administering GH to children with growth retardation caused by glucocorticoid excess is considered (23, 24). It has been suggested that corticosteroids may affect growth through mechanisms involving somatomedins/IGF, either by impairing their biosynthesis or blocking their peripheral action through an increase in somatomedin inhibitors (25). IGF-1 levels are raised by injection of GH (40) and GHRH (41). Various studies have shown no net change in somatomedin levels after glucocorticoid treatment or in patients with Cushing's disease (42, 43). However, in patients with acromegaly a decrease in plasma IGF-I levels was observed after DEX treatment (28), but it is not clear whether free or total IGF-I was measured. In this study we have demonstrated a highly significant increase in total IGF-I concentrations after DEX treatment. The observed increases in IGF-I may simply be due to the increased basal GH levels seen after glucocorticoid treatment. Alternatively, the glucocorticoid-dependent increase in total IGF-I levels may result from interacting peripheral mechanisms regulating both the level of IGF-I synthesis and the concentration of its circulating binding protein. In summary, we have confirmed reports that exogenous glucocorticoid excess leads to an impairment of GHRH-stimulated GH secretion in man and that a similar effect is seen with dopaminergic agents. However, glucocorticoid inhibition of GH responses is not a general phenomenon, as the effect of arginine was significantly enhanced. In addition, we have demonstrated a glucocorticoid-dependent increase in basal GH levels and total plasma IGF-I. Finally, direct comparison of the GH responses obtained after iv administration of a low dose of a new D2-dopamine agonist CV with iv infusion of dopamine have shown that CV is a more effective stimulator of GH release.

JCE & M • 1991 Vol 72 • No 3

Acknowledgments We are indebted to Marco Giacomini, Dora Turnill, and Maria Lopes for their expert technical assistance, and to Dr. R. Rivest and the steroid laboratory for performing the cortisol measurements. The human GHRH employed in this study was a generous gift from Prof. Nicholas Ling. CV 205-502 was supplied by Sandoz Ltd. (Basel, Switzerland) as ampoules ready for iv administration.

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Effects of dexamethasone on growth hormone (GH)-releasing hormone, arginine- and dopaminergic stimulated GH secretion, and total plasma insulin-like growth factor-I concentrations in normal male volunteers.

In man, glucocorticoid treatment and endogenous corticosteroid excess generally suppress stimulated GH release. However, such effects are not entirely...
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