
Circulating oxytocin and vasopressin is influenced by ovarian steroid replacement in women
Author(s) -
Bossmar Thomas,
Forsling Mary,
Åkerlund M.
Publication year - 1995
Publication title -
acta obstetricia et gynecologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.401
H-Index - 102
eISSN - 1600-0412
pISSN - 0001-6349
DOI - 10.3109/00016349509024387
Subject(s) - endocrinology , medicine , vasopressin , oxytocin , estrogen , posterior pituitary , medroxyprogesterone , hormone , medroxyprogesterone acetate , progestogen , pituitary gland
Background : The posterior pituitary hormones appear to be involved in the etiology of primary dysmenorrhoea, but mechanisms regulating their release, particularly the influence of ovarian steroids, are not fully understood. Methods. The effect of 17β‐estradiol and medroxyprogesterone alone and in combination on oxytocin and vasopressin levels was therefore studied in 10 postmenopausal women. Results. Transdermal treatment with estradiol alone by means of patches in a dose of 100 ug/ 24 h for five days resulted in an elevation of the mean plasma concentration of this hormone from undetectable to 262 pmol/1 and increase in mean circulating levels of vasopressin from 0.82 to 1.22 pmol/1 and of oxytocin from 2.50 to 3.98 pmol/1. Oral administration of medroxyprogesterone in a dose of 10 mg per day for 5 days, which resulted in a mean plasma level of 4.3 nmol/I, suppressed vasopressin concentrations to 0.60 pmol/1. When given after five days of treatment with estradiol, medroxyprogesterone also antagonized the stimulatory effect of the estrogen on vasopressin secretion. Medroxyprogesterone alone increased the plasma oxytocin concentration to 3.26 pmol/1, but the progestogen did not significantly influence the stimulatory effect of estradiol on oxytocin secretion. Conclusions. It is concluded that posterior pituitary hormone secretion is influenced by estradiol and progestogens, and that this may be a mechanism for the involvement of ovarian hormones in the etiology of primary dysmenorrhoea.