Effect of Metoclopramide on Serum GH Levels in Normal Women

Chiodera, P.; Coiro,; Zanardi, G; Volpi, R.; Valenti, Giorgio; Butturini, U

doi:10.1055/s-2007-1018937

Cited by 10 publications

(7 citation statements)

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“…In fact, several reports showed increased GH secretion after DA2 blockade or direct dopaminergic stimulation [6,7,10,14]. However, those studies differ from the present study in their characterization of the study group and methodology.…”

Section: Discussioncontrasting

confidence: 61%

“…A previous study with normal women reports an increase in serum GH levels after administration of 10 mg of metoclopramide [10]. However, in contrast to our method, those authors did not control other variables that could affect their results (IGF-I, estradiol, insulin and glucose).…”

Section: Discussionmentioning

confidence: 78%

“…However, under certain conditions characterized by low androgen or increased estrogen levels (such as cirrhosis), GH secretion increases after metoclopramide administration [8,11,12]. In normal women, children, and adolescents, an increase in GH secretion has been shown after metoclopramide infusion, probably due to an estrogen co-stimulatory effect [9,10]. In turn, prolactin (PRL) secretion is stimulated by dopaminergic blockade even in normal populations, and it can be used to study the dopaminergic tonus in some endocrinological disorders [7,13,14].…”

Section: Introductionmentioning

confidence: 99%

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Growth Hormone and Prolactin Secretion after Metoclopramide Administration (DA2 Receptor Blockade) in Fertile Women*

Cunha-Filho¹,

Gross²,

Vettori³

et al. 2001

Horm Metab Res

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In this report, we will describe the results of a cross-sectional study to assess PRL and GH secretion during the early follicular phase in 22 fertile patients after metoclopramide administration in order to achieve a dopaminergic DA2 receptor blockade. Blood samples were collected at - 15, 0, 15, 30, 45 and 60 minutes. PRL, GH, estradiol, IGF-I, TSH, glucose, and insulin were measured in the samples taken at - 15 and 0 minutes. The existence of a correlation between GH and PRL secretion was investigated. All patients presented normal serum levels of estradiol, prolactin, insulin, fasting glucose and IGF-I. Serum GH levels were not changed after metoclopramide infusion (p = 0.302), but there was a significant alteration in serum PRL (p = 0.0001) with the highest levels after 30 (mean: 237.20 ng/ml +/- 95.86) and 45 (mean: 211.80 ng/ml +/- 83.24) minutes. Serum GH levels did not correlate with serum PRL levels after the dopaminergic DA2 blockade. We conclude that GH secretion was not modulated by a direct effect of type 2 dopamine receptor.

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Section: Discussioncontrasting

confidence: 61%

Section: Discussionmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 99%

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Growth Hormone and Prolactin Secretion after Metoclopramide Administration (DA2 Receptor Blockade) in Fertile Women*

Cunha-Filho¹,

Gross²,

Vettori³

et al. 2001

Horm Metab Res

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“…The lack of GH release after MET administration suggests that the inhibitory role of DA on GH release is not active in pregnant women. These results seem to negate also the importance of the absolute estrogen levels in mediating the GH response to MET as suggested in previous observation (Cohen et al 1979;Chiodera et al 1982). During the last trimester of pregnancy reduced GH response has been observed following insulin induced hypoglycaemia and L-arginine infusion (Yen, Vela and Tsai 1970;Samaan, Goplerud and Bradbury 1970).…”

Section: Resultsmentioning

confidence: 59%

Failure of Metoclopramide to Release GH in Pregnant Women

et al. 1983

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Dopaminergic pathways are involved in the control of GH release in man (Scanlon, Pourmand, McGregor, Rodriguez-Arnao, Hall, Gomez-Pan and Hall 1979). In conditions with increased estrogen blood levels an inhibitory role of Dopamine (DA) on GH secretion has been suggested by the evidence that the administration of Metoclopramide (MET) a dopaminergic receptor blocking drug, causes a rapid increment of GH serum concentrations (Cohen, Hay, Beastall and Thomson 1979; Chiodera, Coiro, Zanardi, Volenti and Butturini 1982). This finding led to suggest a possible role of estrogen in modulating the control of GH release (Scanlon et al. 1979). Estrogens in pregnant women have been reported to be elevated. Thus it was of interest to study in this condition the GH response to MET. Materials and Methods111 normal at term pregnant women were studied at parturition with their consent. During labour 10 mg of MET were injected as a bolus in 86 women. Maternal samples (MS) were obtained before MET administration (Basal) and at the parturition time (Treated). The remaining 25 women (Control) received 2 ml of saline and MS were collected only at delivery. Serum GH was measured using materials obtained by Biodata (Milan). In this assay the cross reactivity with hPL is 0.1%. For statistical evaluation, serum samples were divided in 7 groups, 1-7, according to the time interval between MET injection and parturition. The GH values of each group measured at parturition were compared to those obtained before MET administration using the analysis of variance split-plot factorial design. GH level obtained in Control group was compared to the values of the above groups. Results and DiscussionGH concentration of the seven groups of patients before and after MET treatment are reported in table 1. As shown no significant variation of GH levels have been observed in any group at various intervals after MET administration. In Control, GH level measured at the parturition was 5.3 ±0.3 ng/ml. This value was not different from those determined in the Basal and Treated groups. The lack of GH release after MET administration suggests that the inhibitory role of DA on GH release is not active in pregnant women. These results seem to negate also the importance of the absolute estrogen levels in mediating the GH response to MET as suggested in previous observation (Cohen et al. 1979;Chiodera et al. 1982). During the last trimester of pregnancy reduced GH response has been observed following insulin induced hypoglycaemia and L-arginine infusion (Yen, Vela and Tsai 1970;Samaan, Goplerud and Bradbury 1970). The mechanisms responsible for the blunted GH response to releasing tests are only speculative. It should be considered that in pregnancy the high estrogen levels, which facilitate GH release (Vela and Yen 1969) are opposed by high concentrations of progestins, which suppress GH release to insulin and arginine (Bhatia, Moore and Kalkhoff 1972). Thus it is likely that in pregnancy the net result of the estrogen and progestins actions on GH secretion may ...

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“…However, the administration of DAantagonists yields conflicting results : no effect (L'Hermite et al 1978 ; Cavagnini et al 1980) or an augmentation of plasma GII levels (Cohen et al 1979a, b ;Chiodera et al 1982) was reported.…”

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confidence: 99%

The dopaminergic regulation of plasma growth hormone secretion in normal subjects.

Hanew

Sato

Sasaki

et al. 1986

Tohoku J. Exp. Med.

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The role of endogenous dopamine (DA) on plasma GH secretion was studied using domperidone (DA receptor blocker which does not cross blood brain barrier) in 16 normal subjects. After a bolus injection of domperidone (10 mg, iv.), plasma PRL in 11 cases rose quickly and markedly from the basal level of 9.5+ 1.2 ng/ml (Mean+s.E.) to a maximum of 76.3+ 10.6 ng/ml at 30 min. In contrast, plasma GH in these cases showed a delayed and slight increases to domperidone injection where the values at 90 min and 120 min (3.5+0.8 ng/ml and 3.7+1.0 ng/ml) were significantly higher than those in control study (1.2±0.2 ng/ml and 1.0 ±0.1 ng/ml ; p <0.05; n=8). Domperidone infusion (0.22 mg/min/3 hr) was performed in the remaining 5 subjects. The plasma PRL responses were similar to those in the bolus injection of domperidone. These PRL responses were not modified when L-dopa was administered 30 min after the start of iv infusion of domperidone. Plasma GII showed slight but significant increases 135 min after the infusion compared to control study (4.3± 1.2 ng/ml vs. 1.0+0.1 ng/ml ; p <0.05). By the prior infusion of domperidone plasma GH responses to L-dopa was delayed and blunted, i. e., the occurrence of elevation and peak value of GH delayed by 15 min, and the values at 135 min and 150 min (2.3 ±0.5 ng/ml and 1.5 ±0.2 ng/ml) were significantly lower compared to those in the single L-dopa test (6.3+ 1.2 ng/ml and 5.0+ 1.2 ng/ml ; p <0.02 and 0.05, respectively). These results indicate that in normal subjects L-dopa has stimulatory role on GH secretion mainly at the level of CNS (hypothalamus) and partly at the level of median eminence. It is not plausible that endogenous DA has direct tonic inhibitory effects on pituitary somatotrophs.GH ; domperidone ; L-dopa ; dopamine ; median eminence Human growth hormone (OH) secretion is mainly requlated by hypothalamic OH-releasing hormone (GHRH) and OH-release inhibiting hormone (somatostatin) (Arimura and Culler 1985; Jansson et al. 1985). As plasma OH secretion is impaired in cases with hypothalamic lesion (Chihara et al. 1985), GHRH is thought to be more important than somatostatin in the regulation of OH secretion.

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Effect of Metoclopramide on Serum GH Levels in Normal Women

Cited by 10 publications

References 0 publications

Growth Hormone and Prolactin Secretion after Metoclopramide Administration (DA2 Receptor Blockade) in Fertile Women*

Growth Hormone and Prolactin Secretion after Metoclopramide Administration (DA2 Receptor Blockade) in Fertile Women*

Failure of Metoclopramide to Release GH in Pregnant Women

The dopaminergic regulation of plasma growth hormone secretion in normal subjects.

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