Oral contraceptives reduce menstrual pain but the interaction with vasopressin and prostaglandin F2α, two uterine stimulants related to the condition, is unknown. Ten women with a history of moderate to severe dysmenorrhoea were studied. Repeated blood samples were taken during a first menstrual cycle without treatment, during the first 21 days of a second cycle when they received an oral contraceptive (150 μg levonorgestrel and 30 μg ethynyloestradiol) and on the first or second day of the bleeding following hormonal withdrawal. Measurements were made of plasma concentrations of arginine vasopressin, 15-keto-13,14-dihydroprostaglandin F2α, oestradiol-17β, progesterone, ethynyloestradiol, levonorgestrel, FSH, LH and prolactin, and serum osmolality was measured. Seven of the women rated their discomfort as moderate to severe on the first two menstruations, but as none or light at the withdrawal bleeding; with the rating scale for degree of pain that was used, this decrease in pain was significant (P< 0·001). The plasma concentration of vasopressin in these seven women showed significant variation, with the highest concentrations being obtained at the beginning of the two painful menstruations (3·76 ± 0·76 and 1·75 ± 0·30 (s.e.m.) pmol/l and at ovulation in the control cycle (1·91±0·58 pmol/l). During treatment the concentrations were consistently low, except on the first day of withdrawal bleeding (2·33±0·35 pmol/l). The concentrations of the prostaglandin F2α metabolite showed less variation, but again the values at withdrawal bleeding (271 ± 39 pmol/l) were not different from those obtained over the painful menstruations (255 ± 24 and 217 ± 25 pmol/l. The plasma concentrations of ovarian and adenohypophysial hormones, as well as osmolality, were normal throughout. The remaining three women had no, or only slight, menstrual pain in the control cycle and no menstrual peaks in the concentration of vasopressin or prostaglandin F metabolite. The present results gave no evidence for a reduced release of vasopressin and/or prostaglandin F2α that could explain the beneficial effect of oral contraceptives in dysmenorrhoea. Instead, it is possible that this effect is due to a decreased sensitivity of the uterus to these factors.
J. Endocr. (1987) 115,355–361
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