Inhibition of endogenous catecholamine synthesis augments early follicular phase luteinizing hormone secretion

The physiological role of catecholamines, particularly dopamine and norepinephrine, in the regulation of gonadotropin secretion in humans is unclear. We administered the tyrosine hydroxylase inhibitor α-methyl-p-tyrosine (AMPT, 500 mg at 800 and 1000 h) to five women in the early follicular phase of the menstrual cycle and compared LH secretion patterns to those in five untreated controls. Commencing at 800 h, blood was drawn every 15 min for LH and PRL measurements until 1600 h. AMPT elevated PRL concentrations (mean ± SEM) from a baseline of 14.72 ± 2.51 μg/L to a peak of 102.2 ± 24 μg/L. LH concentrations [21.97 ± 0.56 (AMPT) vs. 13.51 ± 0.16 IU/L (control), P < 0.0001], LH area under the curve [11014 ± 1815 (AMPT) vs. 7009 ± 404 IU·min/L (control), P = 0.05] and LH pulse amplitude [9.99 ± 2.38 (AMPT) vs. 4.03 ± 0.61 IU/L (control), P = 0.04] were all greater in the group in which catecholamine synthesis was inhibited. There was no difference in pulse frequency between the groups (7.4 ± 0.51 vs. 6.6 ± 0.24 pulses/8 h, P > 0.05). We conclude 1) inhibition of endogenous catecholamine synthesis augments LH levels in the early follicular phase, and 2) increased LH secretion during catecholamine synthesis inhibition is due, at least in part, to increased LH pulse amplitude but not increased LH pulse frequency.