Different vasculoprotective roles of NO synthase isoforms in vascular lesion formation in mice.

K. Yogo, Hiroaki Shimokawa, H. Funakoshi, T. Kandabashi, K. Miyata, S. Okamoto, K. Egashira, P. Huang, T. Akaike, A. Takeshita

研究成果: Article査読

75 被引用数 (Scopus)

抄録

NO is known to have several important vasculoprotective actions. Although NO is synthesized by 3 different NO synthase (NOS) isoforms, the vasculoprotective action of individual NOS isoforms remains to be clarified. Permanent ligation of the left common carotid artery was performed in control, endothelial NOS (eNOS) knockout (eNOS-KO), and inducible NOS (iNOS) knockout (iNOS-KO) mice. Four weeks after the procedure, neointimal formation and reduction of cross-sectional vascular area (constrictive remodeling) were noted in the left carotid artery. In the eNOS-KO mice, the extent of neointimal formation was significantly larger than in the control or iNOS-KO mice, whereas the extent of vascular remodeling was the highest in the iNOS-KO mice compared with other 2 strains. Antiplatelet therapy with aspirin or antihypertensive treatment with bunazosin failed to inhibit the accelerated neointimal formation in the eNOS-KO mice. These results indicate that eNOS and iNOS have different vasculoprotective actions against the vascular lesion formation caused by blood flow disruption in vivo: NO derived from eNOS inhibits neointimal formation, whereas NO derived from iNOS suppresses the development of constrictive remodeling.

本文言語English
ページ(範囲)E96-E100
ジャーナルArteriosclerosis, thrombosis, and vascular biology
20
11
DOI
出版ステータスPublished - 2000 11月
外部発表はい

ASJC Scopus subject areas

  • 循環器および心血管医学

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