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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2000-8-1
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pubmed:abstractText |
Experiments were designed to investigate the mechanisms underlying the diabetes-related impairment of the vasodilatations of the perfused mesenteric arterial bed induced by acetylcholine (ACh) and K(+). In streptozotocin (STZ)-diabetic rats, the ACh-induced endothelium-dependent vasodilatation was attenuated. The dose-response curves for ACh in control and diabetic rats were each shifted to the right by N(G)-nitro-L-arginine (L-NOARG) and by isotonic high K(+) (60 mM). The ACh dose-response curves under isotonic high K(+) were not different between control and diabetic rats. We also examined the vasodilatation induced by K(+), which is a putative endothelium-derived hyperpolarizing factor (EDHF). The mesenteric vasodilatation induced by a single administration of K(+) was greatly impaired in STZ-induced diabetic rats. Treatment with charybdotoxin plus apamin abolished the ACh-induced vasodilatation but enhanced the K(+)-induced response in controls and diabetic rats. After pretreatment with ouabain plus BaCl(2), the ACh-induced vasodilatation was significantly impaired and the K(+)-induced relaxation was abolished in both control and diabetic rats. The impairment of the endothelium-dependent vasodilatation of the mesenteric arterial bed seen in STZ-induced diabetic rats may be largely due to a defective vascular response to EDHF. It is further suggested that K(+) is one of the endothelium-derived hyperpolarizing factors and that the vasodilatation response to K(+) is impaired in the mesenteric arterial bed from diabetic rats.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10821782-10078995,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10821782-10519554,
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0007-1188
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
130
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
549-56
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:10821782-Acetylcholine,
pubmed-meshheading:10821782-Animals,
pubmed-meshheading:10821782-Blood Glucose,
pubmed-meshheading:10821782-Cholesterol,
pubmed-meshheading:10821782-Diabetes Mellitus, Experimental,
pubmed-meshheading:10821782-Endothelium, Vascular,
pubmed-meshheading:10821782-Hemodynamics,
pubmed-meshheading:10821782-Insulin,
pubmed-meshheading:10821782-Male,
pubmed-meshheading:10821782-Mesenteric Arteries,
pubmed-meshheading:10821782-Potassium,
pubmed-meshheading:10821782-Rats,
pubmed-meshheading:10821782-Rats, Wistar,
pubmed-meshheading:10821782-Triglycerides,
pubmed-meshheading:10821782-Vasodilation,
pubmed-meshheading:10821782-Vasodilator Agents
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pubmed:year |
2000
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pubmed:articleTitle |
Mechanisms underlying the attenuation of endothelium-dependent vasodilatation in the mesenteric arterial bed of the streptozotocin-induced diabetic rat.
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pubmed:affiliation |
Department of Physiology and Morphology, Institute of Medicinal Chemistry, Hoshi University, Shinagawa-ku, Tokyo 142-8501, Japan.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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