Source:http://linkedlifedata.com/resource/pubmed/id/21666117
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2011-8-31
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| pubmed:abstractText |
Endothelin (ET)-1-mediated vasoconstrictor tone contributes to the development and progression of several adiposity-related conditions, including hypertension and atherosclerotic vascular disease. The aims of the present study were to determine 1) whether endogenous ET-1 vasoconstrictor activity is elevated in overweight and obese adults, and, if so, 2) whether increased ET-1-mediated vasoconstriction contributes to the adiposity-related impairment in endothelium-dependent vasodilation. Seventy-nine adults were studied: 34 normal weight [body mass index (BMI) < 25 kg/m(2)], 22 overweight (BMI ? 25 and < 30 kg/m(2)), and 23 obese (BMI ? 30 kg/m(2)). Forearm blood flow (FBF) responses to intra-arterial infusion of ET-1 (5 pmol/min for 20 min) and selective ET-1 receptor blockade (BQ-123, 100 nmol/min for 60 min) were determined. In a subset of the study population, FBF responses to ACh (4.0, 8.0, and 16.0 ?g·100 ml tissue(-1)·min(-1)) were measured in the absence and presence of selective ET-1 receptor blockade. The vasoconstrictor response to ET-1 was significantly blunted in overweight and obese adults (? 70%) compared with normal weight adults. Selective ET-1 receptor blockade elicited a significant vasodilator response (? 20%) in overweight and obese adults but did not alter FBF in normal weight adults. Coinfusion of BQ-123 did not affect FBF responses to ACh in normal weight adults but resulted in an ? 20% increase (P < 0.05) in ACh-induced vasodilation in overweight and obese adults. These results demonstrate that overweight and obesity are associated with enhanced ET-1-mediated vasoconstriction that contributes to endothelial vasodilator dysfunction and may play a role in the increased prevalence of hypertension with increased adiposity.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Endothelin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides, Cyclic,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Endothelin A,
http://linkedlifedata.com/resource/pubmed/chemical/Vasoconstrictor Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Vasodilator Agents,
http://linkedlifedata.com/resource/pubmed/chemical/cyclo(Trp-Asp-Pro-Val-Leu)
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| pubmed:status |
MEDLINE
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| pubmed:month |
Sep
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| pubmed:issn |
1522-1539
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
301
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
H689-95
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| pubmed:meshHeading |
pubmed-meshheading:21666117-Adiposity,
pubmed-meshheading:21666117-Adult,
pubmed-meshheading:21666117-Aged,
pubmed-meshheading:21666117-Analysis of Variance,
pubmed-meshheading:21666117-Blood Pressure,
pubmed-meshheading:21666117-Body Mass Index,
pubmed-meshheading:21666117-Case-Control Studies,
pubmed-meshheading:21666117-Dose-Response Relationship, Drug,
pubmed-meshheading:21666117-Endothelin-1,
pubmed-meshheading:21666117-Endothelium, Vascular,
pubmed-meshheading:21666117-Female,
pubmed-meshheading:21666117-Forearm,
pubmed-meshheading:21666117-Humans,
pubmed-meshheading:21666117-Infusions, Intravenous,
pubmed-meshheading:21666117-Male,
pubmed-meshheading:21666117-Middle Aged,
pubmed-meshheading:21666117-Obesity,
pubmed-meshheading:21666117-Overweight,
pubmed-meshheading:21666117-Peptides, Cyclic,
pubmed-meshheading:21666117-Receptor, Endothelin A,
pubmed-meshheading:21666117-Regional Blood Flow,
pubmed-meshheading:21666117-Regression Analysis,
pubmed-meshheading:21666117-Time Factors,
pubmed-meshheading:21666117-Vasoconstriction,
pubmed-meshheading:21666117-Vasoconstrictor Agents,
pubmed-meshheading:21666117-Vasodilation,
pubmed-meshheading:21666117-Vasodilator Agents
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| pubmed:year |
2011
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| pubmed:articleTitle |
Enhanced endothelin-1 system activity with overweight and obesity.
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| pubmed:affiliation |
Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder 80309, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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