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Article: Loss of endothelial pertussis toxin-sensitive G protein function in atherosclerotic porcine coronary arteries

TitleLoss of endothelial pertussis toxin-sensitive G protein function in atherosclerotic porcine coronary arteries
Authors
Issue Date1991
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circ.ahajournals.org
Citation
Circulation, 1991, v. 83 n. 2, p. 652-660 How to Cite?
AbstractPertussis toxin, an irreversible inhibitor of some G proteins, inhibits endothelium-dependent relaxations to certain agonists in porcine coronary arteries. In the present study, the effects of the toxin were examined on endothelium-dependent and -independent relaxations of hypercholesterolemic and atherosclerotic porcine coronary arteries to assess the functional state of the endothelial pertussis toxin-sensitive G protein. Male Yorkshire pigs were maintained on either a regular diet (control group, n = 7) or a 2% high-cholesterol diet (cholesterol-fed group, n = 7) for 10 weeks. After the initial 2 weeks of maintenance, animals in both groups underwent balloon catheter removal of the endothelium of the left anterior descending or left circumflex coronary arteries. Endothelium-dependent responses were examined in vitro after 10 weeks of maintenance; at this time, a full lining of endothelial cells in both left coronary arteries was confirmed histologically. In arteries with endothelium of the control group (normal responses), pertussis toxin significantly inhibited the endothelium-dependent relaxations to serotonin, UK14304 (a selective α2-adrenergic receptor agonist), and thrombin but not those to ABP, bradykinin, or the calcium ionophore A23187. In previously denuded arteries of the control group (effects of endothelial regeneration alone) or intact arteries of the cholesterol-fed group (effects of hypercholesterolemia alone), the relaxations to serotonin, UK14304, and thrombin were impaired significantly; those relaxations were impaired further in previously denuded arteries of the cholesterol-fed group (effects of atherosclerosis). The inhibitory effects of pertussis toxin were significantly reduced after endothelial regeneration and in hypercholesterolemia and were almost absent in atherosclerosis. Direct relaxations of coronary vascular smooth muscle evoked by nitric oxide or sodium nitroprusside were not significantly affected by either hypercholesterolemia or atherosclerosis. These results indicate that the function of endothelial pertussis toxin-sensitive G protein is impaired in regenerated endothelial cells or hypercholesterolemia and is almost absent in atherosclerosis, accounting in part for the endothelial dysfunction under those pathological conditions.
Persistent Identifierhttp://hdl.handle.net/10722/171028
ISSN
2015 Impact Factor: 17.047
2015 SCImago Journal Rankings: 7.853
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorShimokawa, Hen_US
dc.contributor.authorFlavahan, NAen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:53Z-
dc.date.available2012-10-30T06:11:53Z-
dc.date.issued1991en_US
dc.identifier.citationCirculation, 1991, v. 83 n. 2, p. 652-660en_US
dc.identifier.issn0009-7322en_US
dc.identifier.urihttp://hdl.handle.net/10722/171028-
dc.description.abstractPertussis toxin, an irreversible inhibitor of some G proteins, inhibits endothelium-dependent relaxations to certain agonists in porcine coronary arteries. In the present study, the effects of the toxin were examined on endothelium-dependent and -independent relaxations of hypercholesterolemic and atherosclerotic porcine coronary arteries to assess the functional state of the endothelial pertussis toxin-sensitive G protein. Male Yorkshire pigs were maintained on either a regular diet (control group, n = 7) or a 2% high-cholesterol diet (cholesterol-fed group, n = 7) for 10 weeks. After the initial 2 weeks of maintenance, animals in both groups underwent balloon catheter removal of the endothelium of the left anterior descending or left circumflex coronary arteries. Endothelium-dependent responses were examined in vitro after 10 weeks of maintenance; at this time, a full lining of endothelial cells in both left coronary arteries was confirmed histologically. In arteries with endothelium of the control group (normal responses), pertussis toxin significantly inhibited the endothelium-dependent relaxations to serotonin, UK14304 (a selective α2-adrenergic receptor agonist), and thrombin but not those to ABP, bradykinin, or the calcium ionophore A23187. In previously denuded arteries of the control group (effects of endothelial regeneration alone) or intact arteries of the cholesterol-fed group (effects of hypercholesterolemia alone), the relaxations to serotonin, UK14304, and thrombin were impaired significantly; those relaxations were impaired further in previously denuded arteries of the cholesterol-fed group (effects of atherosclerosis). The inhibitory effects of pertussis toxin were significantly reduced after endothelial regeneration and in hypercholesterolemia and were almost absent in atherosclerosis. Direct relaxations of coronary vascular smooth muscle evoked by nitric oxide or sodium nitroprusside were not significantly affected by either hypercholesterolemia or atherosclerosis. These results indicate that the function of endothelial pertussis toxin-sensitive G protein is impaired in regenerated endothelial cells or hypercholesterolemia and is almost absent in atherosclerosis, accounting in part for the endothelial dysfunction under those pathological conditions.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circ.ahajournals.orgen_US
dc.relation.ispartofCirculationen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Artery Disease - Physiopathologyen_US
dc.subject.meshCoronary Vessels - Drug Effects - Physiopathologyen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Physiopathologyen_US
dc.subject.meshHypercholesterolemia - Physiopathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Contraction - Physiologyen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshPertussis Toxinen_US
dc.subject.meshSwineen_US
dc.subject.meshVirulence Factors, Bordetella - Pharmacologyen_US
dc.titleLoss of endothelial pertussis toxin-sensitive G protein function in atherosclerotic porcine coronary 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.pmid1991383-
dc.identifier.scopuseid_2-s2.0-0026058284en_US
dc.identifier.volume83en_US
dc.identifier.issue2en_US
dc.identifier.spage652en_US
dc.identifier.epage660en_US
dc.identifier.isiWOS:A1991EW94000031-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridShimokawa, H=16684837100en_US
dc.identifier.scopusauthoridFlavahan, NA=7006398882en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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