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Dopaminergic Mechanisms and Luteinizing Hormone Secretion. I. Acute Administration of the Dopamine Agonist Bromocriptine Does Not Inhibit Luteinizing Hormone Release in Hyperprolactinemic Women^*

Division of Endocrinology and Metabolism, Departments of Internal Medicine and Pediatrics,University of Virginia, School of Medicine Charlottesville, Virginia 22908

Address requests for reprints to: Dr. M. O. Thorner, Box 252,University of Virginia Medical Center, Charlottesville, Virginia 22908.

The concept that dopaminergic mechanisms control LH secretion by modulation of gonadotropin-releasing hormone (GnRH) has been recently investigated in man. Since hyperprolactinemia is associated with increased hypothalamic dopamine turnover (which may reflect increased dopaminergic ctivity), inhibition of GnRH by dopamine in this situation would be maximal. Additional stimulation of dopamine receptors by a dopamine agonist would not be expected to result in further inhibition of LH release. Twelve hyperprolactinemic women were studied on 2 days during which measurements of serum PRL and LH were made over 11.5 h. Day 1 served as a control for day 2 when 2.5 mg of the dopamine agonist bromocriptine were administered orally at 0900 h. While serum PRL and LH levels on day 1 showed small fluctuations (±10%), serum PRL on day 2 fell by 82%. Serum LH concentrations on day 2 remained unchanged. The demonstration of the efficacy of bromocriptine in lowering PRL levels documents the expected increase in dopaminergic tone; however, the lack of effect of bromocriptine in surpressing LH release suggests that either there is already maximal endogenous inhibition of GnRH in hyperprolactinemic women or, alternatively, that dopaminergic mechanisms are unimportant in the control of LH secretion.

^* This work was supported in part by Research Grant CA-07535 from the National Cancer Institute and USPHS General Clinical Research Grant RR-847.

Received March 27, 1979.