Enhanced G-protein coupled receptors-mediated contraction and reduced endothelium-dependent relaxation in hypertension
(2007) In European Journal of Pharmacology 557(2-3). p.186-194- Abstract
- The present study was designed to demonstrate a hypothesis that some G-protein coupled receptors are up-regulated and a dysfunction of endothelium occurs in hypertension. The arteries from hypertensive patients and spontaneously hypertensive rats (SHR) were tested. An in vitro myograph system was used to obtain concentration-contraction curves mediated by endothelin ETA, endothelin ETB, 5-hydroxytryptamine 2A (5HT(2A))-receptors and alpha(1)-adrenoceptors in the arterial segments. In hypertensive patients, the maximum contractions (E-max) induced by endothelin ETB, endothelin ETA and 5-HT receptors were significantly increased with elevated pEC(50) values, while a significantly leftward shift of alpha(1)-adrenoceptor-mediated contraction... (More)
- The present study was designed to demonstrate a hypothesis that some G-protein coupled receptors are up-regulated and a dysfunction of endothelium occurs in hypertension. The arteries from hypertensive patients and spontaneously hypertensive rats (SHR) were tested. An in vitro myograph system was used to obtain concentration-contraction curves mediated by endothelin ETA, endothelin ETB, 5-hydroxytryptamine 2A (5HT(2A))-receptors and alpha(1)-adrenoceptors in the arterial segments. In hypertensive patients, the maximum contractions (E-max) induced by endothelin ETB, endothelin ETA and 5-HT receptors were significantly increased with elevated pEC(50) values, while a significantly leftward shift of alpha(1)-adrenoceptor-mediated contraction was seen. Similar results were obtained in SHR. Specific antagonists for 5-HT2A receptors or alpha(1)-adrenoceptors rightward shifted the concentration-contractile curves induced by 5-HT or noradrenalin, while the Emax were not significantly altered, suggesting that the contractions were mediated by 5-HT2A receptors and ocl-adrenoceptors, respectively. Endothelium-dependent maximum relaxation (R-max) in the arterial segments induced by acetylcholine was significantly decreased in both hypertensive patients and SHR. In addition, nitric oxide- and endothelium-derived hyperpolarizing factor-mediated dilatations were decreased significantly and the arterial enclothelial cells were in part lost in SHR. In conclusion, endotheliD ETB, endothelin ETA, 5-HT2A receptor- and alpha-adrenoceptor-mediated contractions were increased in hypertension, while the endotheliurn and its ftinctions were damaged. (c) 2006 Elsevier B.V All rights reserved. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/673751
- author
- Li, He ; Cao, Yong-Xiao ; Liu, Hao and Xu, Cang-Bao LU
- organization
- publishing date
- 2007
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- endothelin receptor, 5-HT receptor, endothelium, alpha(1)-adrenoceptor, hypertension
- in
- European Journal of Pharmacology
- volume
- 557
- issue
- 2-3
- pages
- 186 - 194
- publisher
- Elsevier
- external identifiers
-
- wos:000244494400015
- scopus:33846821685
- pmid:17204265
- ISSN
- 1879-0712
- DOI
- 10.1016/j.ejphar.2006.11.057
- language
- English
- LU publication?
- yes
- id
- cb976cef-3f0b-4236-8326-b8803bbb99ff (old id 673751)
- date added to LUP
- 2016-04-01 11:36:09
- date last changed
- 2024-01-07 13:30:54
@article{cb976cef-3f0b-4236-8326-b8803bbb99ff,
abstract = {{The present study was designed to demonstrate a hypothesis that some G-protein coupled receptors are up-regulated and a dysfunction of endothelium occurs in hypertension. The arteries from hypertensive patients and spontaneously hypertensive rats (SHR) were tested. An in vitro myograph system was used to obtain concentration-contraction curves mediated by endothelin ETA, endothelin ETB, 5-hydroxytryptamine 2A (5HT(2A))-receptors and alpha(1)-adrenoceptors in the arterial segments. In hypertensive patients, the maximum contractions (E-max) induced by endothelin ETB, endothelin ETA and 5-HT receptors were significantly increased with elevated pEC(50) values, while a significantly leftward shift of alpha(1)-adrenoceptor-mediated contraction was seen. Similar results were obtained in SHR. Specific antagonists for 5-HT2A receptors or alpha(1)-adrenoceptors rightward shifted the concentration-contractile curves induced by 5-HT or noradrenalin, while the Emax were not significantly altered, suggesting that the contractions were mediated by 5-HT2A receptors and ocl-adrenoceptors, respectively. Endothelium-dependent maximum relaxation (R-max) in the arterial segments induced by acetylcholine was significantly decreased in both hypertensive patients and SHR. In addition, nitric oxide- and endothelium-derived hyperpolarizing factor-mediated dilatations were decreased significantly and the arterial enclothelial cells were in part lost in SHR. In conclusion, endotheliD ETB, endothelin ETA, 5-HT2A receptor- and alpha-adrenoceptor-mediated contractions were increased in hypertension, while the endotheliurn and its ftinctions were damaged. (c) 2006 Elsevier B.V All rights reserved.}},
author = {{Li, He and Cao, Yong-Xiao and Liu, Hao and Xu, Cang-Bao}},
issn = {{1879-0712}},
keywords = {{endothelin receptor; 5-HT receptor; endothelium; alpha(1)-adrenoceptor; hypertension}},
language = {{eng}},
number = {{2-3}},
pages = {{186--194}},
publisher = {{Elsevier}},
series = {{European Journal of Pharmacology}},
title = {{Enhanced G-protein coupled receptors-mediated contraction and reduced endothelium-dependent relaxation in hypertension}},
url = {{http://dx.doi.org/10.1016/j.ejphar.2006.11.057}},
doi = {{10.1016/j.ejphar.2006.11.057}},
volume = {{557}},
year = {{2007}},
}