Failure of Metoclopramide to Release GH in Pregnant Women

Abstract

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 ...