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Article: Hypercholesterolemia causes generalized impairment of endothelium-dependent relaxation to aggregating platelets in porcine arteries

TitleHypercholesterolemia causes generalized impairment of endothelium-dependent relaxation to aggregating platelets in porcine arteries
Authors
Issue Date1989
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jac
Citation
Journal Of The American College Of Cardiology, 1989, v. 13 n. 6, p. 1402-1408 How to Cite?
AbstractThe role of the endothelium in response to aggregating platelets was examined in porcine coronary and peripheral (carotid, femoral and renal) arteries from normal and hypercholesterolemic pigs. Male Yorkshire pigs were fed either a normal diet or a 2% high cholesterol diet for 10 weeks. Endothelium-dependent responses were examined in vitro. In all arteries from control animals, aggregating platelets caused endothelium-dependent relaxations, which were augmented by ketanserin (a 5-HT2-serotonergic blocker), attenuated by apyrase (an adenosine diphosphatase and triphosphatase) or methiothepin (a combined 5-HT1 and 5-HT2-serotonergic blocker) and were almost abolished by a combination of apyrase and methiothepin. The platelet-induced relaxations were most pronounced in the coronary arteries. Adenosine diphosphate caused endothelium-dependent relaxations, which were significantly attenuated by apyrase. Serotonin also caused endothelium-dependent relaxations, which were significantly attenuated by methiothepin but augmented by ketanserin. The endothelium-dependent relaxations to adenosine diphosphate were most pronounced in coronary arteries and those to serotonin in coronary and renal arteries. In cholesterol-fed animals, the endothelium-dependent relaxations to aggregating platelets, adenosine diphosphate and serotonin were impaired in all four arteries. These experiments indicate that 1) the endothelium exerts inhibitory effects against aggregating platelets in porcine coronary and peripheral arteries; 2) platelet-induced endothelium-dependent relaxations are achieved by purinergic and 5-HT1-serotonergic receptors on the endothelium; and 3) hypercholesterolemia reduces the endothelium-dependent relaxations to aggregating platelets in a generalized manner because it impairs the relaxations to adenosine diphosphate and serotonin released from the platelets.
Persistent Identifierhttp://hdl.handle.net/10722/170955
ISSN
2015 Impact Factor: 17.759
2015 SCImago Journal Rankings: 10.097
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorShimokawa, Hen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:36Z-
dc.date.available2012-10-30T06:11:36Z-
dc.date.issued1989en_US
dc.identifier.citationJournal Of The American College Of Cardiology, 1989, v. 13 n. 6, p. 1402-1408en_US
dc.identifier.issn0735-1097en_US
dc.identifier.urihttp://hdl.handle.net/10722/170955-
dc.description.abstractThe role of the endothelium in response to aggregating platelets was examined in porcine coronary and peripheral (carotid, femoral and renal) arteries from normal and hypercholesterolemic pigs. Male Yorkshire pigs were fed either a normal diet or a 2% high cholesterol diet for 10 weeks. Endothelium-dependent responses were examined in vitro. In all arteries from control animals, aggregating platelets caused endothelium-dependent relaxations, which were augmented by ketanserin (a 5-HT2-serotonergic blocker), attenuated by apyrase (an adenosine diphosphatase and triphosphatase) or methiothepin (a combined 5-HT1 and 5-HT2-serotonergic blocker) and were almost abolished by a combination of apyrase and methiothepin. The platelet-induced relaxations were most pronounced in the coronary arteries. Adenosine diphosphate caused endothelium-dependent relaxations, which were significantly attenuated by apyrase. Serotonin also caused endothelium-dependent relaxations, which were significantly attenuated by methiothepin but augmented by ketanserin. The endothelium-dependent relaxations to adenosine diphosphate were most pronounced in coronary arteries and those to serotonin in coronary and renal arteries. In cholesterol-fed animals, the endothelium-dependent relaxations to aggregating platelets, adenosine diphosphate and serotonin were impaired in all four arteries. These experiments indicate that 1) the endothelium exerts inhibitory effects against aggregating platelets in porcine coronary and peripheral arteries; 2) platelet-induced endothelium-dependent relaxations are achieved by purinergic and 5-HT1-serotonergic receptors on the endothelium; and 3) hypercholesterolemia reduces the endothelium-dependent relaxations to aggregating platelets in a generalized manner because it impairs the relaxations to adenosine diphosphate and serotonin released from the platelets.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jacen_US
dc.relation.ispartofJournal of the American College of Cardiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Factors - Physiologyen_US
dc.subject.meshCarotid Arteries - Physiologyen_US
dc.subject.meshCoronary Vessels - Physiologyen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshFemoral Artery - Physiologyen_US
dc.subject.meshHypercholesterolemia - Physiopathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle, Smooth, Vascular - Physiologyen_US
dc.subject.meshNitric Oxideen_US
dc.subject.meshPlatelet Aggregationen_US
dc.subject.meshRenal Artery - Physiologyen_US
dc.subject.meshSwineen_US
dc.subject.meshVascular Resistanceen_US
dc.titleHypercholesterolemia causes generalized impairment of endothelium-dependent relaxation to aggregating platelets in porcine arteriesen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/0735-1097(89)90318-5-
dc.identifier.pmid2784807-
dc.identifier.scopuseid_2-s2.0-0024555403en_US
dc.identifier.volume13en_US
dc.identifier.issue6en_US
dc.identifier.spage1402en_US
dc.identifier.epage1408en_US
dc.identifier.isiWOS:A1989U337400026-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridShimokawa, H=16684837100en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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