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Sodium nitrite therapy rescues ischemia-induced neovascularization and blood flow recovery in hypertension

DC Field Value Language
dc.contributor.author최수경-
dc.date.accessioned2018-05-10T06:36:00Z-
dc.date.available2018-05-10T06:36:00Z-
dc.date.issued2012-
dc.identifier.issn0031-6768-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/158276-
dc.description.abstractArterial hypertension is a major risk factor that can lead to complication of peripheral vascular disease due, in part, to endothelial dysfunction. Because sodium nitrite (SN) can be converted to nitric oxide (NO), which counteracts endothelial dysfunction, we explored the effect of nitrite on neovascularization following hind limb ischemia in different models of hypertension (HT). Chronic delivery of angiotensin II (Ang II, 400 ng/kg/min) or N(omega)-nitro-L-arginine-methyl-ester (L-NAME, 0.1 g/L) was used for a 2-week period to induce hypertension. Mice were subjected to femoral artery ligation-induced ischemia in the hind limb followed by treatment with SN (50 mg/L) for 2 weeks. SN significantly reduced systolic arterial blood pressure in mice receiving Ang II and L-NAME but had no effect in sham animals. After 2 weeks, blood flow and microangiography showed 60 % ± 1.0 recovery in sham compared with 40 % ± 1.3 in HT mice. Importantly, sham and HT mice treated with SN showed a 100 % blood flow recovery associated with normalization in capillary density. The inhibition of xanthine-oxido-reductase (allopurinol) or VEGFR (SU-5416) prevented the neovascularization in HT mice treated with SN. Cyclic GMP (cGMP) content in the hind limb was significantly increased in mice treated with SN compared with non-treated mice. Nitrite/nitrate content was only increased in the sham group treated with SN. Immunoprecipitation and Western blot analysis revealed an increase in eNOS/Akt/VEGFR phosphorylation in skeletal muscle from mice treated with SN compared with non-treated mice. Our findings indicate that SN therapy rescues the neovascularization and blood flow recovery in the ischemic hind limb of sham and HT mice likely through the Akt/NO/cGMP and VEGFR pathways.-
dc.description.statementOfResponsibilityopen-
dc.languageGerman, English-
dc.publisherSpringer-
dc.relation.isPartOfPFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAllopurinol/pharmacology-
dc.subject.MESHAngiotensin II/pharmacology-
dc.subject.MESHAnimals-
dc.subject.MESHArterial Pressure/drug effects-
dc.subject.MESHCapillaries/drug effects-
dc.subject.MESHCapillaries/physiopathology-
dc.subject.MESHCyclic AMP/metabolism-
dc.subject.MESHCyclic GMP/metabolism-
dc.subject.MESHFemoral Artery/drug effects-
dc.subject.MESHFemoral Artery/metabolism-
dc.subject.MESHFemoral Artery/physiopathology-
dc.subject.MESHHindlimb/blood supply*-
dc.subject.MESHHindlimb/drug effects-
dc.subject.MESHHindlimb/metabolism-
dc.subject.MESHHypertension/drug therapy*-
dc.subject.MESHHypertension/physiopathology*-
dc.subject.MESHIndoles/pharmacology-
dc.subject.MESHIschemia/drug therapy*-
dc.subject.MESHIschemia/metabolism-
dc.subject.MESHIschemia/physiopathology-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHMuscle, Skeletal/blood supply-
dc.subject.MESHMuscle, Skeletal/drug effects-
dc.subject.MESHMuscle, Skeletal/metabolism-
dc.subject.MESHNG-Nitroarginine Methyl Ester/pharmacology-
dc.subject.MESHNeovascularization, Pathologic/drug therapy-
dc.subject.MESHNeovascularization, Pathologic/metabolism-
dc.subject.MESHNeovascularization, Pathologic/physiopathology-
dc.subject.MESHNitric Oxide/metabolism-
dc.subject.MESHNitric Oxide Synthase Type III/metabolism-
dc.subject.MESHProto-Oncogene Proteins c-akt/metabolism-
dc.subject.MESHPyrroles/pharmacology-
dc.subject.MESHReceptors, Vascular Endothelial Growth Factor/antagonists & inhibitors-
dc.subject.MESHReceptors, Vascular Endothelial Growth Factor/metabolism-
dc.subject.MESHRegional Blood Flow/drug effects*-
dc.subject.MESHSodium Nitrite/pharmacology*-
dc.subject.MESHXanthine Dehydrogenase/antagonists & inhibitors-
dc.subject.MESHXanthine Dehydrogenase/metabolism-
dc.titleSodium nitrite therapy rescues ischemia-induced neovascularization and blood flow recovery in hypertension-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Physiology-
dc.contributor.googleauthorAli Amin-
dc.contributor.googleauthorSookyoung Choi-
dc.contributor.googleauthorYehia Osman-Elazeik-
dc.contributor.googleauthorNariman Badr El-Din-
dc.contributor.googleauthorChristopher G. Kevil-
dc.contributor.googleauthorLouis G. Navar-
dc.contributor.googleauthorPhilip Kadowitz-
dc.contributor.googleauthorMohamed Trebak-
dc.contributor.googleauthorKhalid Matrougui-
dc.identifier.doi10.1007/s00424-012-1167-y-
dc.contributor.localIdA04091-
dc.relation.journalcodeJ02502-
dc.identifier.eissn1432-2013-
dc.identifier.pmid23053479-
dc.contributor.alternativeNameChoi, Soo Kyoung-
dc.contributor.affiliatedAuthorChoi, Soo Kyoung-
dc.citation.volume464-
dc.citation.number6-
dc.citation.startPage583-
dc.citation.endPage592-
dc.identifier.bibliographicCitationPFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, Vol.464(6) : 583-592, 2012-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers

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