SynopsisThe effect of chronic administration of sulpiride on serum human growth hormone (hGH), prolactin and thyroid stimulating hormone (TSH) was examined in 6 normal subjects. Sulpiride was given orally at a dose of 300 mg (t. i. d.) for 30 days. Sulpiride raised serum prolactin levels in all subjects examined.In addition, sulpiride suppressed hGH release induced by L-dopa, although the basal hGH level was not changed.Sulpiride treatment appeared to antagonize partially the inhibitory effect of L-dopa on prolactin release.Following thyrotropin-releasing hormone (TRH) injection, the percent increment in prolactin levels from the baseline in sulpiridetreated subjects was less than in controls without sulpiride. In contrast, both the basal and TRH-stimulated TSH levels were not influenced by sulpiride.These observations suggest that sulpiride suppressses L-dopa-induced hGH release and stimulates prolactin release, presumably by acting against the dopaminergic mechanism, either on the hypothalamus or on the pituitary.The decreased prolactin response to TRH after sulpiride treatment may indicate a diminished reserve capacity in pituitary prolactin release.

Adult male wistar rats averaging 200 g each were subjected to food removal for 1--6 days or fed ad libitum throughout (controls). Plasma GH levels and pituitary GH contents were measured by radioimmunoassay. The GH responses to intravenous injection of TRH (2.5 microgram/100 g B.W.), PGE1(5 microgram/100 g B.W.), LH-RH (1 microgram/100 g B.W.) and Chlorpromazine (CPZ, 100 microgram/100 g B.W.) were tested under urethane anesthesia. Circulating GH levels were significantly increased by prolonged starvation, while pituitary GH contents progressively decreased with increased periods of starvation. In addition, following the TRH administration, plasma GH levels increased in starved rats compared to the control rats. A similar effect was also observed with PGE1. In contrast, the administration of CPZ, which was reported to act at the hypothalamic level, failed to potentiate GH release in starved rats under urethane anesthesia. These observations suggest an increased susceptibility of starved rats to urethane anesthesia with the administration of TRH and PGE1 in the GH secretory mechanism. In addition, the fact that no further potentiation of GH release was observed by CPZ treatment may indicate an abnormality of the hypothalamic dopaminergic mechanism in starved animals.

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