Endothelium-derived prostanoids reduce 5-hydroxytryptamine-induced contraction in the human uterine artery
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1113829
- author
- Karlsson, C ; Bodelsson, Gunilla LU ; Bodelsson, Mikael LU and Stjernquist, Martin LU
- organization
- publishing date
- 1998
- 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
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Research Unit for Urogynaecology and Reproductive Pharmacology (013242710), Division of Infection Medicine (BMC) (013024020), Pediatrics/Urology/Gynecology/Endocrinology (013240400)
- 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
- 2016-04-01 12:16:29
- date last changed
- 2022-01-27 01:22:58
@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}}, keywords = {{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}}, url = {{http://humrep.oxfordjournals.org/cgi/content/abstract/13/7/1947}}, volume = {{13}}, year = {{1998}}, }