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Article: Upregulation of heme oxygenase 1 by hemin impairs endothelium-dependent contractions in the aorta of the spontaneously hypertensive rat

TitleUpregulation of heme oxygenase 1 by hemin impairs endothelium-dependent contractions in the aorta of the spontaneously hypertensive rat
Authors
KeywordsEndothelial dysfunction
Endothelium-dependent contractions
Heme oxygenase 1
Hemin
Prostacyclin
Reactive oxygen species
Spontaneously hypertensive rat
Thromboxane-prostanoid receptor
Issue Date2011
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/
Citation
Hypertension, 2011, v. 58 n. 5, p. 926-934 How to Cite?
AbstractHeme oxygenase converts heme to carbon monoxide, biliverdin (subsequently converted to bilirubin), and free iron. Pharmacological induction of heme oxygenase 1 has an antihypertensive effect in the spontaneously hypertensive rat. The present study investigated whether upregulation of heme oxygenase 1 by hemin reduces endothelial dysfunction in this animal. Thirty-six-week- old rats were divided into a hemin treatment (50 mg/kg, IP injection, once) and a control group. Aortas were isolated for the measurement of isometric tension, production of reactive oxygen species, and heme oxygenase activity, as well as gene and protein expressions. Hemin treatment augmented the expression and activity of heme oxygenase 1. This in vivo induction of heme oxygenase 1, but not in vitro incubation with the heme oxygenase products carbon monoxide or bilirubin, led to an improvement of endothelial function in that acetylcholine-induced relaxations were potentiated and acetylcholine-and calcium ionophore-induced contractions were attenuated. Free radical production was suppressed by hemin treatment, judging from the results of 2',7'- dichlorodihydrofluoresein diacetate staining, dihydroethidium staining, and lucigenin chemiluminescence, which was explained by the decreased expressions of NADPH oxidase 2 and cyclooxygenase 1. The production of prostacyclin was decreased by heme oxygenase 1 induction, which was explained by a lower expression of cyclooxygenase 1. Contractions to vasoconstrictor concentrations of prostacyclin and its mimetic iloprost were attenuated, suggesting that the responsiveness of thromboxane-prostanoid receptors to prostacyclin was decreased in hemin-treated rats. The suppressed production of free radicals and prostacyclin and the decrease of thromboxane-prostanoid receptors sensitivity concur to explain the impairment of endothelium-dependent contractions caused by heme oxygenase 1 induction by hemin. © 2011 American Heart Association, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/146897
ISSN
2015 Impact Factor: 6.294
2015 SCImago Journal Rankings: 3.702
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grant Council (University of Hong Kong)777208M
Research Centre of Heart, Brain, Hormone and Healthy Aging of the University of Hong Kong
World Class UniversityR31-20029
Ministry of Education, Science, and Technology, South Korea
Funding Information:

This research is supported by the Hong Kong Research Grant Council (University of Hong Kong, No. 777208M); by Research Centre of Heart, Brain, Hormone and Healthy Aging of the University of Hong Kong; and by the World Class University program (R31-20029) funded by the Ministry of Education, Science, and Technology, South Korea.

References

 

DC FieldValueLanguage
dc.contributor.authorLi, Zen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2012-05-23T05:48:53Z-
dc.date.available2012-05-23T05:48:53Z-
dc.date.issued2011en_HK
dc.identifier.citationHypertension, 2011, v. 58 n. 5, p. 926-934en_HK
dc.identifier.issn0194-911Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/146897-
dc.description.abstractHeme oxygenase converts heme to carbon monoxide, biliverdin (subsequently converted to bilirubin), and free iron. Pharmacological induction of heme oxygenase 1 has an antihypertensive effect in the spontaneously hypertensive rat. The present study investigated whether upregulation of heme oxygenase 1 by hemin reduces endothelial dysfunction in this animal. Thirty-six-week- old rats were divided into a hemin treatment (50 mg/kg, IP injection, once) and a control group. Aortas were isolated for the measurement of isometric tension, production of reactive oxygen species, and heme oxygenase activity, as well as gene and protein expressions. Hemin treatment augmented the expression and activity of heme oxygenase 1. This in vivo induction of heme oxygenase 1, but not in vitro incubation with the heme oxygenase products carbon monoxide or bilirubin, led to an improvement of endothelial function in that acetylcholine-induced relaxations were potentiated and acetylcholine-and calcium ionophore-induced contractions were attenuated. Free radical production was suppressed by hemin treatment, judging from the results of 2',7'- dichlorodihydrofluoresein diacetate staining, dihydroethidium staining, and lucigenin chemiluminescence, which was explained by the decreased expressions of NADPH oxidase 2 and cyclooxygenase 1. The production of prostacyclin was decreased by heme oxygenase 1 induction, which was explained by a lower expression of cyclooxygenase 1. Contractions to vasoconstrictor concentrations of prostacyclin and its mimetic iloprost were attenuated, suggesting that the responsiveness of thromboxane-prostanoid receptors to prostacyclin was decreased in hemin-treated rats. The suppressed production of free radicals and prostacyclin and the decrease of thromboxane-prostanoid receptors sensitivity concur to explain the impairment of endothelium-dependent contractions caused by heme oxygenase 1 induction by hemin. © 2011 American Heart Association, Inc.en_HK
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/en_HK
dc.relation.ispartofHypertensionen_HK
dc.subjectEndothelial dysfunctionen_HK
dc.subjectEndothelium-dependent contractionsen_HK
dc.subjectHeme oxygenase 1en_HK
dc.subjectHeminen_HK
dc.subjectProstacyclinen_HK
dc.subjectReactive oxygen speciesen_HK
dc.subjectSpontaneously hypertensive raten_HK
dc.subjectThromboxane-prostanoid receptoren_HK
dc.titleUpregulation of heme oxygenase 1 by hemin impairs endothelium-dependent contractions in the aorta of the spontaneously hypertensive raten_HK
dc.typeArticleen_HK
dc.identifier.emailWang, Y: yuwanghk@hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityWang, Y=rp00239en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1161/HYPERTENSIONAHA.111.173807en_HK
dc.identifier.pmid21947473-
dc.identifier.scopuseid_2-s2.0-83155175257en_HK
dc.identifier.hkuros199786en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-83155175257&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume58en_HK
dc.identifier.issue5en_HK
dc.identifier.spage926en_HK
dc.identifier.epage934en_HK
dc.identifier.isiWOS:000296588100664-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, Z=54397452700en_HK
dc.identifier.scopusauthoridWang, Y=34973733700en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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