Plosker S M, Rabinovici J, Montalvo M, Jaffe R B
Department of Obstetrics, Gynecology, University of California, San Francisco 94143, USA.
J Clin Endocrinol Metab. 1995 Aug;80(8):2530-3. doi: 10.1210/jcem.80.8.7629255.
The physiological role of hypothalamic catecholamines in the regulation of TSH secretion in humans has not been studied extensively. We administered the catecholamine synthesis inhibitor alpha-methyl-p-tyrosine (AMPT) to five women in the early follicular phase (one of menstrual cycle days 2-5) of the menstrual cycle and compared TSH secretion patterns to those in five women at the same time in the cycle who did not receive AMPT. From 0800-1600 h, volunteers had an i.v. line placed, through which blood was withdrawn every 15 min for TSH and PRL determinations. AMPT (500 mg) was administered to the study group at 0800 h and again at 1000 h. Baseline TSH concentrations at 0800 h were not significantly different between the control and treatment groups. In keeping with its characteristic circadian secretion pattern, TSH in the control group was 1.72 +/- 0.23 mIU/L at 0800 h, declined to 1.02 +/- 0.11 mIU/L by 1600 h, and was significantly less than the 0800 h value at all time points beyond 1115 h. The decline in TSH was observed in all five controls. By contrast, TSH in the AMPT group rose from an 0800 h value of 1.99 +/- 0.09 mIU/L to a peak of 3.30 +/- 0.86 IU/L by 1245 h, and was significantly higher than that at 0800 h in the treated group from 1130-1315 h. The increase in TSH was observed in all five women who received AMPT. There were significant differences between the mean TSH concentrations in the AMPT-treated (2.51 +/- 0.09 mIU/L) vs. the control group (1.28 +/- 0.09 mIU/L; P < 0.0001) for the entire study. The effectiveness of AMPT was demonstrated by an elevation of mean PRL concentrations from a baseline of 16.67 +/- 2.55 micrograms/L to a peak of 138.7 +/- 21.6 micrograms/L. We conclude that endogenous catecholamines tonically inhibit TSH secretion in the early follicular phase. These data suggest modulation of TRH by tuberoinfundibular dopamine at the hypothalamic and/or pituitary level.