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. 1982 Dec;34(12):2155-62.

[Effects of bromocriptine and dopamine on pituitary hormone secretion in women]

[Article in Japanese]
  • PMID: 6818310

[Effects of bromocriptine and dopamine on pituitary hormone secretion in women]

[Article in Japanese]
K Masaoka et al. Nihon Sanka Fujinka Gakkai Zasshi. 1982 Dec.

Abstract

The present study was designed to examine whether a dopamine agonist, bromocriptine (Brc) exerts similar effects as dopamine (DA) on the pituitary hormones secretion and also to investigate the interaction of these dopaminergic agents and a dopamine receptor antagonist, metoclopramide (MCP) on the DA receptors in the hypothalamic-pituitary axis. Thirty normal cycling women in the midfollicular phase volunteered for this study. Following the administration of Brc (2.5mg, orally) to 13 subjects, a partially significant fall in LH levels, but not in FSH levels, during 4h was observed. DA, infused at a rate of 5 micrograms/kg/min for 4h, induced a significant fall in LH levels between 1 and 4h, but in FSH levels only at 2.5h after the start of infusion in 9 subjects. The amplitude of the spontaneous pulsations of LH secretion which was observed in 8 control subjects, was diminished by DA, while the amplitude seemed to be augmented by Brc. The administration of MCP (10mg, i.v.) to all subjects at 3h during the 4h experimental period caused no observable change in LH and FSH levels. A significant and progressive decline in PRL levels was observed in both Brc-and DA-treated groups of subjects, and this PRL-lowering effect was markedly counteracted by MCP administration in DA-treated group, but not in Brc-treated group. Brc induced a widely varying but significant rise in GH levels, with which MCP did not appear to interfere, whereas DA failed to cause any significant changes in GH levels. These data suggest that Brc, in contrast with DA, seems to be able to increase the pulse amplitude, but not the basal level, of LH and to stimulate GH secretion. Brc is also regarded to be a potent and unique PRL inhibitor, because its PRL-lowering effect cannot be easily antagonized by MCP.

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