Stimulation of vasopressin release in women with primary dysmenorrhoea and after oral contraceptive treatment—effect on uterine contractility

Abstract

Objective To study aspects of the aetiology of primary dysmenorrhoea and mechanisms underlying the therapeutic effect in this condition of an oral contraceptive. Intervention Intrauterine pressure was recorded before and during infusion of hypertonic saline (5% NaCl, 0.06 ml/kg/min) over 75 min on the first day of bleeding in women with dysmenorrhoea and after 3 weeks of oral contraceptive treatment. Plasma sampling every 15 min of ongoing infusion for the estimation of osmolality, arginine vasopressin, oxytocin and the prostaglandin (PG) F‐metabolito, 15‐keto‐13, 14‐dihydro‐PGF2α. Subjects Ten healthy nulliparous women with moderate to severe primary dysmenorrhoea. Main outcome measures Plasma levels of posterior pituitary hormones and the PGF‐metabolite. Total pressure area (TPA) of the recording curve. Results In dysmenorrhoea before infusion the plasma concentration of vasopressin was in mean 2.18, oxytocin 5.05 and the PGF‐metabolite 321.5 pmol/1, and the TPA 3.8 kPa ≥ 10 min. After oral contraceptive treatment the vasopressin level and the TPA were significantly reduced. At both sessions apart from intensifying the pain, the saline infusion increased vasopressin and oxytocin levels as well as the TPA, whereas the concentration of the PGF‐metabolite at both sessions decreased. Conclusion Confirmation is provided of the elevated secretion of arginine vasopressin and PGF2α, as well as increased uterine activity in primary dysmenorrhoea. The observations are in agreement with the concept that a lowered level of vasopressin and a decreased uterine activity contributes to the beneficial effect of OCs in the condition. Stimulation of the secretion of vasopressin increases the uterine activity and symptoms of primary dysmenorrhoea, but results suggest that this effect does not involve a mechanism of increased PGF‐synthesis. The role of oxytocin in dysmenorrhoea can not yet be defined.

Anxious–Retarded Depression: Relation with Plasma Vasopressin and Cortisol

“…In exploratory analyses we confirmed that oral contraceptives decrease plasma vasopressin levels (Ekstrom et al, 1992;Kostoglou-Athanassiou et al, 1998) and increase plasma cortisol levels (Amin et al, 1980). Therefore, 15 patients taking oral contraceptives were excluded, as were patients with depression in relation to panic disorder.…”

Avaliação do funcionamento do eixo HPA em deprimidos por meio de medidas basais: revisão sistemática da literatura e análise das metodologias utilizadas

“…Sabe-se que, em alguns estudos, os pacientes usaram benzodiazepínicos, porém estes podem inibir o CRH e suprimir a secreção de cortisol e ACTH. Segundo Ekstrom et al 59 e Kostoglou-Athanassiou et al 60 , o uso de contraceptivo oral diminui o nível plasmático de vasopressina (substância que exerce influência no eixo HPA), e segundo Amin et al 61 , há aumento do nível de cortisol. Em alguns estudos, o uso de droga antipsicótica pode influenciar o nível de cortisol e arginina-vasopressina plasmático 62,63 .…”

The effect of relcovaptan (SR 49059), an orally active vasopressin V1areceptor antagonist, on uterine contractions in preterm labor

“…Relcovaptan inhibits vasopressin-induced uterine contractions in nonpregnant healthy volunteers [12]. It also prevents pain of primary dysmenorrhea [13], a condition in which increased vasopressin release is apparently of etiological importance [14][15][16]. In the present study we investigated the effect of blocking vasopressin V 1a receptors by orally administrated relcovaptan on uterine contractions in women with preterm labor.…”