Uterine prostaglandins seem to be important in the production of myometrial hyperactivity and uterine ischemia in primary dysmenorrhea. Other factors, however, might be involved in the genesis of this condition, and their mechanisms of action could include ultimate prostaglandin synthesis and release. One such factor is arginine vasopressin. In a recent study, an elevated plasma level of vasopressin was found in women with primary dysmenorrhea, but it was not clear whether this was of etiological importance in the condition or whether the increased secretion of the hormone resulted from menstrual pain. In the present investigation, a prostaglandin synthesis inhibitor was given to women with primary dysmenorrhea to determine the effect of pain relief on vasopressin levels in this condition.Nine women with severe primary dysmenorrhea and eight healthy controls with no menstrual pain were included in the study. Samples of venous blood were collected on the morning of the first day of menstruation, 2 to 10 hours after onset. After the first series of samples had been obtained, the women with dysmenorrhea were given naproxen orally at a dose of 500 mg. The women were instructed to report on the effects, and the sampling procedure was repeated after 60 to 90 minutes.At the time of the second sampling, all dysmenorrheic women reported practically no pain, and had experienced no side effects of the drug. The vasopressin level, which before treatment was 1.71 ± 0.43 μU/ml (mean ± SE), remained virtually unchanged after treatment (1.89 ± 0.46 μU/ml). On both occasions, the concentrations were significantly higher than that in the controls (0.51 ± 0.15 μU/ml; P 0.005). Neither the plasma sodium concentration (141 ± 0.8 mmol/liter) nor the plasma osmolality (290 ± 2.0 mOsm/liter) differed significantly from those of the controls (141 ± 1.1 mmol/liter and 296 ± 7.2 mOsm/liter, respectively).All women had ovulated, as judged by the plasma progesterone and estradiol concentrations in the midluteal phase of the menstrual cycle preceding vasopressin sampling. In dysmenorrheic women, the concentrations (mean ± SE) of progesterone and estradiol at this time in the cycle were 8.52 ± 0.97 ng/ml and 185 ± 4.5 pg/ml, respectively, which values were not significantly different from the concentrations of 8.69 ± 0.98 ng/ml and 164 ± 4.3 pg/ml, respectively, in the controls. There was little correlation between vasopressin levels on day 1 and progesterone and estradiol concentrations in the midluteal phase in dysmenorrheic women (r= —0.13 and —0.40, respectively) and in controls (r= —0.24 and —0.30, respectively).On the 1 st day of menstruation, the progesterone and estradiol concentrations in plasma (mean ± SE) were 0.38 ± 0.2 ng/ml and 62 ± 2.6 pg/ml, respectively, in dysmenorrheic women, and 70 ± 2.8 pg/ml, respectively, in controls. The differences between the two groups were not significant. The vasopressin concentrations were not related to the progesterone and estradiol concentrations (r= —0.45 and 0.15, respectively, in dysmenorrheic women;r= 0.58 and —0.29, respectively, in controls).
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