Heat stress alters G-protein coupled receptor-mediated function and endothelium-dependent relaxation in rat mesenteric artery
(2008) In European Journal of Pharmacology 588(2-3). p.280-285- Abstract
- Heat stress has been demonstrated to have strong cardiovascular effects. However, the underlying mechanism-mediated cardiovascular effects are still not fully understood. The present study was designed to examine if heat stress alters vascular G-protein coupled receptor-mediated vasomotion and endothelium function in rat mesenteric artery. Rats were divided into two groups, heat stress rats and control. The G-protein coupled receptors of endothelin type B (ETB) receptor-, endothelin type A (ETA) receptor-, 5-hydroxytryptamine (5-HT) receptor-, calcitonin gene-related peptide (CGRP) receptor-, alpha-adrenoceptor-mediated vosoactivity and endothelium-dependent relaxation on rat mesenteric artery ring segments were monitored by a myograph... (More)
- Heat stress has been demonstrated to have strong cardiovascular effects. However, the underlying mechanism-mediated cardiovascular effects are still not fully understood. The present study was designed to examine if heat stress alters vascular G-protein coupled receptor-mediated vasomotion and endothelium function in rat mesenteric artery. Rats were divided into two groups, heat stress rats and control. The G-protein coupled receptors of endothelin type B (ETB) receptor-, endothelin type A (ETA) receptor-, 5-hydroxytryptamine (5-HT) receptor-, calcitonin gene-related peptide (CGRP) receptor-, alpha-adrenoceptor-mediated vosoactivity and endothelium-dependent relaxation on rat mesenteric artery ring segments were monitored by a myograph system. The plasma level of CGRP was determined by radioimmunological assay. Compared with control arterial segments, the contractile response curves of sarafotoxin 6c, a selective ETB receptor agonist and 5-HT in the arterial segments from heat stress rats were shifted towards left. An increased maximum contraction (E-max) induced by sarafotoxin 6c, but not 5-HT, was seen in the arterial segments from heat stress rats. CGRP-incluced relaxation in endothelium-denuded arterial segments from heat stress rats was enhanced. The relaxation in endothelium-intact arterial segments induced by acetylcholine was significantly decreased in heat stress rats. In addition, the plasma concentration of CGRP was increased in heat stress rats. The endothelium-dependent relaxation was characterized and shown there was a decrease in nitric oxide and endothelium-derived hyperpolarising factor-mediated relaxation in the arterial segments from heat stress rats. In conclusion, heat stress induces an enhanced vascular endothelin ETB-, 5-HT-receptors-mediated contraction, an enhanced CGRP-receptor-induced relaxation and damage to endothelium-dependent relaxation. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1186966
- author
- Li, Jie ; Cao, Yong-Xiao ; Cao, Lei ; Liu, Yong and Xu, Cang-Bao LU
- organization
- publishing date
- 2008
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- mesenteric artery, gene-related peptide, calcitonin, 5-hydroxytryptamine, heat stress, sarafatoxin 6c
- in
- European Journal of Pharmacology
- volume
- 588
- issue
- 2-3
- pages
- 280 - 285
- publisher
- Elsevier
- external identifiers
-
- wos:000257187600021
- scopus:44649126658
- ISSN
- 1879-0712
- DOI
- 10.1016/j.ejphar.2008.04.038
- language
- English
- LU publication?
- yes
- id
- 2e3b608b-32ff-4422-915e-98beabed6765 (old id 1186966)
- date added to LUP
- 2016-04-01 12:00:58
- date last changed
- 2024-01-08 05:04:19
@article{2e3b608b-32ff-4422-915e-98beabed6765,
abstract = {{Heat stress has been demonstrated to have strong cardiovascular effects. However, the underlying mechanism-mediated cardiovascular effects are still not fully understood. The present study was designed to examine if heat stress alters vascular G-protein coupled receptor-mediated vasomotion and endothelium function in rat mesenteric artery. Rats were divided into two groups, heat stress rats and control. The G-protein coupled receptors of endothelin type B (ETB) receptor-, endothelin type A (ETA) receptor-, 5-hydroxytryptamine (5-HT) receptor-, calcitonin gene-related peptide (CGRP) receptor-, alpha-adrenoceptor-mediated vosoactivity and endothelium-dependent relaxation on rat mesenteric artery ring segments were monitored by a myograph system. The plasma level of CGRP was determined by radioimmunological assay. Compared with control arterial segments, the contractile response curves of sarafotoxin 6c, a selective ETB receptor agonist and 5-HT in the arterial segments from heat stress rats were shifted towards left. An increased maximum contraction (E-max) induced by sarafotoxin 6c, but not 5-HT, was seen in the arterial segments from heat stress rats. CGRP-incluced relaxation in endothelium-denuded arterial segments from heat stress rats was enhanced. The relaxation in endothelium-intact arterial segments induced by acetylcholine was significantly decreased in heat stress rats. In addition, the plasma concentration of CGRP was increased in heat stress rats. The endothelium-dependent relaxation was characterized and shown there was a decrease in nitric oxide and endothelium-derived hyperpolarising factor-mediated relaxation in the arterial segments from heat stress rats. In conclusion, heat stress induces an enhanced vascular endothelin ETB-, 5-HT-receptors-mediated contraction, an enhanced CGRP-receptor-induced relaxation and damage to endothelium-dependent relaxation.}},
author = {{Li, Jie and Cao, Yong-Xiao and Cao, Lei and Liu, Yong and Xu, Cang-Bao}},
issn = {{1879-0712}},
keywords = {{mesenteric artery; gene-related peptide; calcitonin; 5-hydroxytryptamine; heat stress; sarafatoxin 6c}},
language = {{eng}},
number = {{2-3}},
pages = {{280--285}},
publisher = {{Elsevier}},
series = {{European Journal of Pharmacology}},
title = {{Heat stress alters G-protein coupled receptor-mediated function and endothelium-dependent relaxation in rat mesenteric artery}},
url = {{http://dx.doi.org/10.1016/j.ejphar.2008.04.038}},
doi = {{10.1016/j.ejphar.2008.04.038}},
volume = {{588}},
year = {{2008}},
}