Linked Life Data

17140857

Source:http://linkedlifedata.com/resource/pubmed/id/17140857

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2007-1-29
pubmed:abstractText
Previous studies have shown that heat stress possesses cardioprotection, which is related to the synthesis and release of calcitonin gene-related peptide (CGRP) via activation of capsaicin receptor (vanilloid receptor subtype 1, VR1) on the capsaicin-sensitive sensory neurons. The VR1 exists in human umbilical vein endothelial cells (HUVECs). Endothelial cells can synthesize CGRP and CGRP could protect against endothelial dysfunction induced by lysophosphatidylcholine (LPC) or oxidized low-density lipoprotein. In the present study, we explored whether the endothelial cell-derived CGRP is involved in the effect of heat stress on endothelial function in vivo and in vitro. Our results indicated that heat stress significantly increased the plasma concentration of CGRP, which was abolished by pretreatment with capsazepine, a VR1 antagonist. Immunohistochemistry and in situ hybridization showed that the endothelium of mesenteric artery and aorta expressed CGRP. And heat stress increased the expression of CGRP, which was also abolished by capsazepine. LPC attenuated the endothelium-dependent relaxation responses of aorta rings, which were improved by pretreatment with heat stress. In cultured HUVECs, the CGRP secretion was increased after heat stress. LPC increased the lactate dehydrogenase (LDH) activity in the cultured medium and decreased the cell viability, suggesting that LPC injured the HUVECs. However, pretreatment with heat stress attenuated the injurious effects of LPC on HUVECs. And this beneficial effect of heat stress on HUVECs was inhibited by capsazepine or CGRP(8-37), the CGRP receptor antagonist. The present results suggest that the endothelial cell-derived CGRP contributes to the protective effects of heat stress on endothelial function. Our study provides a potential mechanism to explain the protective effect of heat stress on cardiovascular system.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1537-1891
pubmed:author
pubmed:issnType
Print
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
238-46
pubmed:meshHeading
pubmed-meshheading:17140857-Animals, pubmed-meshheading:17140857-Aorta, Thoracic, pubmed-meshheading:17140857-Calcitonin Gene-Related Peptide, pubmed-meshheading:17140857-Capsaicin, pubmed-meshheading:17140857-Cell Survival, pubmed-meshheading:17140857-Cells, Cultured, pubmed-meshheading:17140857-Disease Models, Animal, pubmed-meshheading:17140857-Endothelial Cells, pubmed-meshheading:17140857-Endothelium, Vascular, pubmed-meshheading:17140857-Heat Stress Disorders, pubmed-meshheading:17140857-Humans, pubmed-meshheading:17140857-Lysophosphatidylcholines, pubmed-meshheading:17140857-Male, pubmed-meshheading:17140857-Mesenteric Arteries, pubmed-meshheading:17140857-Peptide Fragments, pubmed-meshheading:17140857-RNA, Messenger, pubmed-meshheading:17140857-Rats, pubmed-meshheading:17140857-Rats, Sprague-Dawley, pubmed-meshheading:17140857-TRPV Cation Channels, pubmed-meshheading:17140857-Time Factors, pubmed-meshheading:17140857-Vasodilation
pubmed:year
2007
pubmed:articleTitle
Involvement of endothelial cell-derived CGRP in heat stress-induced protection of endothelial function.
pubmed:affiliation
Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, 110 Xiang-Ya Road, Changsha, Hunan, 410078, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't