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Article: Transgenic mice over-expressing et-1 in the endothelial cells develop systemic hypertension with altered vascular reactivity

TitleTransgenic mice over-expressing et-1 in the endothelial cells develop systemic hypertension with altered vascular reactivity
Authors
Issue Date2011
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2011, v. 6 n. 11 How to Cite?
AbstractEndothelin-1 (ET-1) is a potent vasoconstrictor involved in the regulation of vascular tone and implicated in hypertension. However, the role of small blood vessels endothelial ET-1 in hypertension remains unclear. The present study investigated the effect of chronic over-expression of endothelial ET-1 on arterial blood pressure and vascular reactivity using transgenic mice approach. Transgenic mice (TET-1) with endothelial ET-1 over-expression showed increased in ET-1 level in the endothelial cells of small pulmonary blood vessels. Although TET-1 mice appeared normal, they developed mild hypertension which was normalized by the ET A receptor (BQ123) but not by ET B receptor (BQ788) antagonist. Tail-cuff measurements showed a significant elevation of systolic and mean blood pressure in conscious TET-1 mice. The mice also exhibited left ventricular hypertrophy and left axis deviation in electrocardiogram, suggesting an increased peripheral resistance. The ionic concentrations in the urine and serum were normal in 8-week old TET-1 mice, indicating that the systemic hypertension was independent of renal function, although, higher serum urea levels suggested the occurrence of kidney dysfunction. The vascular reactivity of the aorta and the mesenteric artery was altered in the TET-1 mice indicating that chronic endothelial ET-1 up-regulation leads to vascular tone imbalance in both conduit and resistance arteries. These findings provide evidence for the role of spatial expression of ET-1 in the endothelium contributing to mild hypertension was mediated by ET A receptors. The results also suggest that chronic endothelial ET-1 over-expression affects both cardiac and vascular functions, which, at least in part, causes blood pressure elevation. © 2011 Leung et al.
Persistent Identifierhttp://hdl.handle.net/10722/146634
ISSN
2015 Impact Factor: 3.057
2015 SCImago Journal Rankings: 1.395
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grant CouncilHKU 7220/02M
Funding Information:

The present work was supported by a research grant from the Hong Kong Research Grant Council (HKU 7220/02M) to SKC. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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DC FieldValueLanguage
dc.contributor.authorLeung, JWCen_HK
dc.contributor.authorWong, WTen_HK
dc.contributor.authorKoon, HWen_HK
dc.contributor.authorMo, FMen_HK
dc.contributor.authorTam, Sen_HK
dc.contributor.authorHuang, Yen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2012-05-08T03:21:25Z-
dc.date.available2012-05-08T03:21:25Z-
dc.date.issued2011en_HK
dc.identifier.citationPlos One, 2011, v. 6 n. 11en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146634-
dc.description.abstractEndothelin-1 (ET-1) is a potent vasoconstrictor involved in the regulation of vascular tone and implicated in hypertension. However, the role of small blood vessels endothelial ET-1 in hypertension remains unclear. The present study investigated the effect of chronic over-expression of endothelial ET-1 on arterial blood pressure and vascular reactivity using transgenic mice approach. Transgenic mice (TET-1) with endothelial ET-1 over-expression showed increased in ET-1 level in the endothelial cells of small pulmonary blood vessels. Although TET-1 mice appeared normal, they developed mild hypertension which was normalized by the ET A receptor (BQ123) but not by ET B receptor (BQ788) antagonist. Tail-cuff measurements showed a significant elevation of systolic and mean blood pressure in conscious TET-1 mice. The mice also exhibited left ventricular hypertrophy and left axis deviation in electrocardiogram, suggesting an increased peripheral resistance. The ionic concentrations in the urine and serum were normal in 8-week old TET-1 mice, indicating that the systemic hypertension was independent of renal function, although, higher serum urea levels suggested the occurrence of kidney dysfunction. The vascular reactivity of the aorta and the mesenteric artery was altered in the TET-1 mice indicating that chronic endothelial ET-1 up-regulation leads to vascular tone imbalance in both conduit and resistance arteries. These findings provide evidence for the role of spatial expression of ET-1 in the endothelium contributing to mild hypertension was mediated by ET A receptors. The results also suggest that chronic endothelial ET-1 over-expression affects both cardiac and vascular functions, which, at least in part, causes blood pressure elevation. © 2011 Leung et al.en_HK
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshArteries - metabolism - physiology-
dc.subject.meshBlood Pressure - physiology-
dc.subject.meshEndothelial Cells - metabolism-
dc.subject.meshEndothelin-1 - genetics - metabolism-
dc.subject.meshHypertension - genetics - metabolism-
dc.titleTransgenic mice over-expressing et-1 in the endothelial cells develop systemic hypertension with altered vascular reactivityen_HK
dc.typeArticleen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1371/journal.pone.0026994en_HK
dc.identifier.pmid22096514-
dc.identifier.pmcidPMC3214015-
dc.identifier.scopuseid_2-s2.0-80855133584en_HK
dc.identifier.hkuros200010-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80855133584&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume6en_HK
dc.identifier.issue11en_HK
dc.identifier.isiWOS:000297553900017-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectCharacterization of endothelin-1 gene manipulated mice for ischemic stroke, a leading cause of death and disability-
dc.identifier.scopusauthoridLeung, JWC=8978634300en_HK
dc.identifier.scopusauthoridWong, WT=35932584500en_HK
dc.identifier.scopusauthoridKoon, HW=6602639908en_HK
dc.identifier.scopusauthoridMo, FM=7005059536en_HK
dc.identifier.scopusauthoridTam, S=7202037323en_HK
dc.identifier.scopusauthoridHuang, Y=34770945300en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK

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