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Hypoxia-augmented constriction of deep femoral artery mediated by inhibition of eNOS in smooth muscle

DC Field Value Language
dc.contributor.author신동민-
dc.date.accessioned2014-12-18T08:25:08Z-
dc.date.available2014-12-18T08:25:08Z-
dc.date.issued2013-
dc.identifier.issn0363-6143-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/86269-
dc.description.abstractIn contrast to the conventional belief that systemic arteries dilate under hypoxia, we found that α-adrenergic contraction of rat deep femoral artery (DFA) is largely augmented by hypoxia (HVC(DFA)) while hypoxia (3% Po(2)) alone had no effect. HVC(DFA) was consistently observed in both endothelium-intact and -denuded vessels with partial pretone by phenylephrine (PhE) or by other conditions (e.g., K(+) channel blocker). Patch-clamp study showed no change in the membrane conductance of DFA myocytes by hypoxia. The RhoA-kinase inhibitor Y27632 attenuated HVC(DFA). The nitric oxide synthase inhibitor [nitro-L-arginine methyl ester (L-NAME)] and soluble guanylate cyclase inhibitor [oxadiazole quinoxalin (ODQ)] strongly augmented the PhE-pretone, while neither of the agents had effect without pretone. NADPH oxidase type 4 (NOX4) inhibitors (diphenylene iodonium and plumbagin) also potentiated PhE-pretone, which was reversed by NO donor. No additive HVC(DFA) was observed under the pretreatment with L-NAME, ODQ, or plumbagin. Western blot and immunohistochemistry analysis showed that both NOX4 and endothelial nitric oxide synthase (eNOS) are expressed in smooth muscle layer of DFA. Various mitochondria inhibitors (rotenone, myxothiazol, and cyanide) prevented HVC(DFA). From the pharmacological data, as a mechanism for HVC(DFA), we suggest hypoxic inhibition of eNOS in myocytes. The putative role of NOX4 and mitochondria requires further investigation. The HVC(DFA) may prevent imbalance between cardiac output and skeletal blood flow under emergent hypoxia combined with increased sympathetic tone.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfAMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHFemoral Artery/enzymology-
dc.subject.MESHFemoral Artery/metabolism*-
dc.subject.MESHFemoral Artery/physiopathology-
dc.subject.MESHHypoxia/enzymology-
dc.subject.MESHHypoxia/metabolism*-
dc.subject.MESHHypoxia/physiopathology-
dc.subject.MESHMale-
dc.subject.MESHMuscle Cells/pathology-
dc.subject.MESHMuscle Cells/physiology-
dc.subject.MESHMuscle, Smooth, Vascular/enzymology-
dc.subject.MESHMuscle, Smooth, Vascular/metabolism*-
dc.subject.MESHNeural Inhibition/physiology*-
dc.subject.MESHNitric Oxide Synthase Type III/antagonists & inhibitors*-
dc.subject.MESHNitric Oxide Synthase Type III/metabolism*-
dc.subject.MESHRats-
dc.subject.MESHRats, Sprague-Dawley-
dc.subject.MESHUncoupling Agents/pharmacology-
dc.subject.MESHVasoconstriction/physiology*-
dc.titleHypoxia-augmented constriction of deep femoral artery mediated by inhibition of eNOS in smooth muscle-
dc.typeArticle-
dc.contributor.collegeCollege of Dentistry (치과대학)-
dc.contributor.departmentDept. of Oral Biology (구강생물학)-
dc.contributor.googleauthorJung-A. Han-
dc.contributor.googleauthorEun Yeoung Seo-
dc.contributor.googleauthorHae Jin Kim-
dc.contributor.googleauthorSu Jung Park-
dc.contributor.googleauthorHae Young Yoo-
dc.contributor.googleauthorJin Young Kim-
dc.contributor.googleauthorDong Min Shin-
dc.contributor.googleauthorJin Kyoung Kim-
dc.contributor.googleauthorYin Hua Zhang-
dc.contributor.googleauthorSung Joon Kim-
dc.identifier.doi10.1152/ajpcell.00176.2012-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02091-
dc.relation.journalcodeJ00102-
dc.identifier.eissn1522-1563-
dc.identifier.pmid23099643-
dc.subject.keywordAnimals-
dc.subject.keywordFemoral Artery/enzymology-
dc.subject.keywordFemoral Artery/metabolism*-
dc.subject.keywordFemoral Artery/physiopathology-
dc.subject.keywordHypoxia/enzymology-
dc.subject.keywordHypoxia/metabolism*-
dc.subject.keywordHypoxia/physiopathology-
dc.subject.keywordMale-
dc.subject.keywordMuscle Cells/pathology-
dc.subject.keywordMuscle Cells/physiology-
dc.subject.keywordMuscle, Smooth, Vascular/enzymology-
dc.subject.keywordMuscle, Smooth, Vascular/metabolism*-
dc.subject.keywordNeural Inhibition/physiology*-
dc.subject.keywordNitric Oxide Synthase Type III/antagonists & inhibitors*-
dc.subject.keywordNitric Oxide Synthase Type III/metabolism*-
dc.subject.keywordRats-
dc.subject.keywordRats, Sprague-Dawley-
dc.subject.keywordUncoupling Agents/pharmacology-
dc.subject.keywordVasoconstriction/physiology*-
dc.contributor.alternativeNameShin, Dong Min-
dc.contributor.affiliatedAuthorShin, Dong Min-
dc.rights.accessRightsfree-
dc.citation.volume304-
dc.citation.number1-
dc.citation.startPage78-
dc.citation.endPage88-
dc.identifier.bibliographicCitationAMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, Vol.304(1) : 78-88, 2013-
dc.identifier.rimsid28881-
dc.type.rimsART-
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers

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