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

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

    研究成果: Contribution to journalArticle査読

    71 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.

    本文言語英語
    ページ(範囲)E96-E100
    ジャーナルArteriosclerosis, thrombosis, and vascular biology
    20
    11
    DOI
    出版ステータス出版済み - 11 2000

    All Science Journal Classification (ASJC) codes

    • Cardiology and Cardiovascular Medicine

    フィンガープリント 「Different vasculoprotective roles of NO synthase isoforms in vascular lesion formation in mice.」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

    引用スタイル