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Endothelium-derived prostanoids reduce 5-hydroxytryptamine-induced contraction in the human uterine artery

Karlsson, C; Bodelsson, Gunilla LU ; Bodelsson, Mikael LU and Stjernquist, Martin LU (1998) In Human Reproduction 13(7). p.1947-1951
Abstract
The contribution of endothelium-linked mechanisms to the contraction induced by 5-hydroxytryptamine (5-HT) was investigated in the isolated human uterine artery. 5-HT contracted the uterine artery concentration-dependently. Removal of the endothelium or treatment with the cyclooxygenase inhibitor indomethacin potentiated the contractile response to 5-HT. The nitric oxide synthase inhibitor L-N(G)-monomethyl-arginine (L-NMMA) did not influence the contraction induced by 5-HT. Indomethacin did not affect the response to 5-HT in endothelium-denuded vessels. The 5-HT1 receptor agonist 5-carboxyamidotryptamine (5-CT) did not relax precontracted arteries. Removal of the endothelium did not change the response to 5-HT in the presence of the... (More)
The contribution of endothelium-linked mechanisms to the contraction induced by 5-hydroxytryptamine (5-HT) was investigated in the isolated human uterine artery. 5-HT contracted the uterine artery concentration-dependently. Removal of the endothelium or treatment with the cyclooxygenase inhibitor indomethacin potentiated the contractile response to 5-HT. The nitric oxide synthase inhibitor L-N(G)-monomethyl-arginine (L-NMMA) did not influence the contraction induced by 5-HT. Indomethacin did not affect the response to 5-HT in endothelium-denuded vessels. The 5-HT1 receptor agonist 5-carboxyamidotryptamine (5-CT) did not relax precontracted arteries. Removal of the endothelium did not change the response to 5-HT in the presence of the 5-HT(1B/D) receptor antagonist GR127935 and the 5-HT1A and 5-HT1B receptor antagonist -pindolol. The 5-HT1B receptor antagonist SB224289 did not affect the contraction induced by 5-HT. The results indicate that the 5-HT-induced contraction in the human uterine artery is accompanied by the release of an endothelium-derived relaxing factor (EDRF). This EDRF seems to be a prostanoid, probably prostacyclin (PGI2). The endothelium-linked mechanism seems to be mediated via a 5-HT1 receptor, but it is not possible to further classify the receptor subtype by the information obtained in this study. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
EDRF/endothelium/5-hydroxytryptamine/prostanoids/ uterine artery
in
Human Reproduction
volume
13
issue
7
pages
1947 - 1951
publisher
Oxford University Press
external identifiers
  • pmid:9740455
  • scopus:0031821439
ISSN
0268-1161
language
English
LU publication?
yes
id
6476fce9-733f-4622-8eb0-bba310bfd302 (old id 1113829)
alternative location
http://humrep.oxfordjournals.org/cgi/content/abstract/13/7/1947
date added to LUP
2008-07-16 12:12:51
date last changed
2017-01-01 04:59:56
@article{6476fce9-733f-4622-8eb0-bba310bfd302,
  abstract     = {The contribution of endothelium-linked mechanisms to the contraction induced by 5-hydroxytryptamine (5-HT) was investigated in the isolated human uterine artery. 5-HT contracted the uterine artery concentration-dependently. Removal of the endothelium or treatment with the cyclooxygenase inhibitor indomethacin potentiated the contractile response to 5-HT. The nitric oxide synthase inhibitor L-N(G)-monomethyl-arginine (L-NMMA) did not influence the contraction induced by 5-HT. Indomethacin did not affect the response to 5-HT in endothelium-denuded vessels. The 5-HT1 receptor agonist 5-carboxyamidotryptamine (5-CT) did not relax precontracted arteries. Removal of the endothelium did not change the response to 5-HT in the presence of the 5-HT(1B/D) receptor antagonist GR127935 and the 5-HT1A and 5-HT1B receptor antagonist -pindolol. The 5-HT1B receptor antagonist SB224289 did not affect the contraction induced by 5-HT. The results indicate that the 5-HT-induced contraction in the human uterine artery is accompanied by the release of an endothelium-derived relaxing factor (EDRF). This EDRF seems to be a prostanoid, probably prostacyclin (PGI2). The endothelium-linked mechanism seems to be mediated via a 5-HT1 receptor, but it is not possible to further classify the receptor subtype by the information obtained in this study.},
  author       = {Karlsson, C and Bodelsson, Gunilla and Bodelsson, Mikael and Stjernquist, Martin},
  issn         = {0268-1161},
  keyword      = {EDRF/endothelium/5-hydroxytryptamine/prostanoids/
uterine artery},
  language     = {eng},
  number       = {7},
  pages        = {1947--1951},
  publisher    = {Oxford University Press},
  series       = {Human Reproduction},
  title        = {Endothelium-derived prostanoids reduce 5-hydroxytryptamine-induced contraction in the human uterine artery},
  volume       = {13},
  year         = {1998},
}