Source:http://linkedlifedata.com/resource/pubmed/id/12105142
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2002-7-9
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pubmed:abstractText |
Although insulin-mediated vasodilation is impaired in insulin resistance, the mechanisms of this are unknown. We investigated factors mediating vasoactive responses to insulin in control and insulin-resistant rats. Responses to insulin in small mesenteric arteries from control and insulin-resistant rats were investigated after blocking endothelin-A receptors, cyclooxygenase, nitric oxide synthase, and potassium channels. In addition, insulin's effect on prostacyclin production in small mesenteric blood vessels was assessed by enzyme immunoassay. Insulin induced a concentration-dependent vasodilation in control arteries that was absent in arteries from insulin-resistant rats. However, in the presence of BQ610, an endothelin-A receptor antagonist, the response to insulin was normalized in insulin-resistant arteries. In control arteries, insulin-induced vasodilation was completely inhibited by indomethacin, meclofenamate, glibenclamide, or potassium chloride. In contrast, neither n-nitro-L-arginine nor the combination of charybdotoxin and apamin altered vasodilation to insulin. In insulin-resistant arteries in the presence of BQ610, vasodilation was also inhibited by indomethacin, glibenclamide, and potassium chloride. Insulin increased prostacyclin production in small mesenteric blood vessels from both groups of rats to a similar degree. Insulin-induced vasodilation in small rat mesenteric arteries is mediated through prostacyclin- and ATP-dependent potassium channels. However, insulin-resistant arteries do not vasodilate to insulin unless endothelin-A receptors are blocked. Thus, impaired relaxation to insulin in insulin-resistant rats is due to enhanced vasoconstriction by endothelin, which offsets a normal vasodilatory response to insulin.
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pubmed:grant | |
pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/6-Ketoprostaglandin F1 alpha,
http://linkedlifedata.com/resource/pubmed/chemical/BQ 610,
http://linkedlifedata.com/resource/pubmed/chemical/Endothelins,
http://linkedlifedata.com/resource/pubmed/chemical/Glyburide,
http://linkedlifedata.com/resource/pubmed/chemical/Indomethacin,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Oligopeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Endothelin A,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Endothelin
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1524-4563
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
40
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
78-82
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:12105142-6-Ketoprostaglandin F1 alpha,
pubmed-meshheading:12105142-Animals,
pubmed-meshheading:12105142-Dose-Response Relationship, Drug,
pubmed-meshheading:12105142-Endothelins,
pubmed-meshheading:12105142-Glyburide,
pubmed-meshheading:12105142-Indomethacin,
pubmed-meshheading:12105142-Insulin,
pubmed-meshheading:12105142-Insulin Resistance,
pubmed-meshheading:12105142-Male,
pubmed-meshheading:12105142-Mesenteric Artery, Superior,
pubmed-meshheading:12105142-Oligopeptides,
pubmed-meshheading:12105142-Potassium Chloride,
pubmed-meshheading:12105142-Rats,
pubmed-meshheading:12105142-Rats, Sprague-Dawley,
pubmed-meshheading:12105142-Receptor, Endothelin A,
pubmed-meshheading:12105142-Receptors, Endothelin,
pubmed-meshheading:12105142-Vasodilation
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pubmed:year |
2002
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pubmed:articleTitle |
Enhanced endothelin activity prevents vasodilation to insulin in insulin resistance.
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pubmed:affiliation |
Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA. amiller@wfubmc.edu
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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