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Involvement of prostaglandins in vasopressin stimulation of the human uterus
Author(s) -
STRÖMBERG P.,
ÅKERLUND M.,
FORSLING M. L.,
KINDAHL H.
Publication year - 1983
Publication title -
bjog: an international journal of obstetrics and gynaecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.157
H-Index - 164
eISSN - 1471-0528
pISSN - 1470-0328
DOI - 10.1111/j.1471-0528.1983.tb08919.x
Subject(s) - uterus , vasopressin , endocrinology , medicine , oxytocin , stimulation , menstruation , arginine , naproxen , hormone , chemistry , amino acid , biochemistry , alternative medicine , pathology
The involvement of prostaglandins (PG) in the vasopressin (VP) action on the human uterus was investigated in healthy women during three menstruations. Intrauterine pressure was recorded and total pressure area measured. Repeated plasma samples were taken for estimations of arginine(A)‐ and lysine(L)‐VP, 15‐keto‐13,14‐dihydro‐PGF 2α and 11‐ ketotetranor PGF metabolites. During the first menstruation LVP was infused in a dose of 0.08 μg/min. During the second menstruation the infusion of LVP was repeated with the same dose, but 70 min before infusion the women received an oral dose of 500 mg of naproxen. During the third menstruation PGF 2α was administered intravenously in a dose of 25 μg/min. LVP infusion per se caused a significant increase in uterine activity and plasma levels of LVP and PG metabolites. When the women were pretreated with naproxen practically the same uterine activity was induced and closely similar plasma levels of LVP were obtained, but the levels of PG metabolites decreased significantly in comparison with the first series of experiments. Infusion of PGF 2α caused an increase in uterine activity but no change in the plasma levels of AVP. The results indicate that uterine stimulation with VP is possible without an obligatory last step of PG synthesis and release. The results also support the concept that an elevated VP level in primary dysmenorrhoea may be of aetiological importance and is not just released as a 'stress'‐hormone because of the dysmenorrhoeic pain.