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Endothelin-1 stimulates prostaglandin F2 alpha release from human endometrium.

Authors
  • Cameron, I T
  • Davenport, A P
  • Brown, M J
  • Smith, S K
Type
Published Article
Journal
Prostaglandins Leukotrienes and Essential Fatty Acids
Publisher
Elsevier
Publication Date
Mar 01, 1991
Volume
42
Issue
3
Pages
155–157
Identifiers
PMID: 1857721
Source
Medline
License
Unknown

Abstract

Despite a key role in the pathogenesis of menorrhagia, the factors controlling the uterine vascular bed are poorly understood. This study has assessed the effects of the potent vasoconstrictor endothelin (ET)-1 on prostaglandin (PG) release from human endometrial explants in short-term culture. There was no significant difference between the production of PGF2 alpha in proliferative and secretory tissue (1709 and 2434 pg/mg/h--median values, range 70,3745 and 219,6700 pg/mg/h). Less PGE was released than PGF2 alpha, and the amount did not vary with the phase of the menstrual cycle (308 and 296 pg/mg/h (range 65,387 and 105,429) for proliferative and secretory tissue). ET-1 (10 and 100 nM) and arachidonic acid (AA, 30 microM), stimulated PGF2 alpha release from proliferative, but not secretory endometrium, by 78%, 86% (P less than 0.01) and 80% respectively, compared with control tissue. No effect was seen on PGE release. ET-1 may play a role in the local control of the endometrial vascular bed either directly, or via the release of PGF2 alpha.

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