title: 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.
  
  
  METHODS
  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-metabolite, 15-keto-13,14-dihydro-PGF2 alpha.
  
  
  METHODS
  Ten healthy nulliparous women with moderate to severe primary dysmenorrhoea.
  
  
  METHODS
  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/l, and the TPA 3.8 kPa x 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.
  
  
  CONCLUSIONS
  Confirmation is provided of the elevated secretion of arginine vasopressin and PGF2 alpha, 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.
authors.affiliation: Department of Obstetrics and Gynecology, University Hospital, Lund, Sweden.
authors.forename: P
authors.initials: P
authors.lastname: Ekström
authors.forename: M
authors.initials: M
authors.lastname: Akerlund
authors.forename: M
authors.initials: M
authors.lastname: Forsling
authors.forename: H
authors.initials: H
authors.lastname: Kindahl
authors.forename: T
authors.initials: T
authors.lastname: Laudanski
authors.forename: G
authors.initials: G
authors.lastname: Mrugacz
mesh_terms: D000328:Adult; D001127:Arginine Vasopressin / Q000097:blood*; D003278:Contraceptives, Oral, Hormonal / Q000097:blood / Q000627:therapeutic use*; D004412:Dysmenorrhea / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D004997:Ethinyl Estradiol / Q000097:blood / Q000627:therapeutic use*; D019304:Ethinyl Estradiol-Norgestrel Combination; D005260:Female; D006801:Humans; D009644:Norgestrel / Q000097:blood / Q000627:therapeutic use*; D011312:Pressure; D014590:Uterine Contraction / Q000187:drug effects*
chemical_list: D003278:Contraceptives, Oral, Hormonal; D001127:Arginine Vasopressin; D009644:Norgestrel; D004997:Ethinyl Estradiol; D019304:Ethinyl Estradiol-Norgestrel Combination