Involvement of prostaglandins in vasopressin stimulation of the human uterus
Article first published online: 23 AUG 2005
DOI: 10.1111/j.1471-0528.1983.tb08919.x
Issue
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BJOG: An International Journal of Obstetrics & Gynaecology
Volume 90, Issue 4, pages 332–337, April 1983
Additional Information
How to Cite
STRÖMBERG, P., ÅKERLUND, M., FORSLING, M. L. and KINDAHL, H. (1983), Involvement of prostaglandins in vasopressin stimulation of the human uterus. BJOG: An International Journal of Obstetrics & Gynaecology, 90: 332–337. doi: 10.1111/j.1471-0528.1983.tb08919.x
Publication History
- Issue published online: 23 AUG 2005
- Article first published online: 23 AUG 2005
- Received 30 A ugust 1982 Accepted 20 October 1982
- Abstract
- References
- Cited By
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-PGF2α 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 PGF2α 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 PGF2α 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.

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