Epidermal Growth Factor Induces Vasoconstriction Through the Phosphatidylinositol 3-Kinase-Mediated Mitogen-Activated Protein Kinase Pathway in Hypertensive Rats

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著者

    • Kim Junghwan KIM Junghwan
    • Department of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University
    • KIM Hyo Jin
    • Department of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University
    • SO Hyun Ha
    • Department of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University
    • LEE Keun Sang
    • Department of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University
    • LEE Hwan Myung
    • Department of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University
    • ROH Hui Yul
    • Department of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University
    • CHOI Wahn Soo
    • Department of Immunology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University
    • PARK Tae Kyu
    • Department of Biotechnology, College of Biomedical & Health Science, Konkuk University
    • KIM Bokyung
    • Department of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University

抄録

We investigated whether increased contractile responsiveness to epidermal growth factor (EGF) is associated with altered activation of mitogen-activated protein kinase (MAPK) in the aortic smooth muscle of deoxycorticosterone acetate (DOCA)-salt hypertensive rats. EGF induced contraction and MAPK activity in aortic smooth muscle strips, which were significantly increased in tissues from the DOCA-salt hypertensive rats compared with those from sham-operated rats. AG1478, PD98059, and LY294002, inhibitors of EGF receptor (EGFR) tyrosine kinase, MAPK/extracellular signal-regulated kinase (ERK) kinase, and phosphatidylinositol 3-kinase (PI3K), respectively, inhibited the contraction and the activity of ERK1/2 that were elevated by EGF. Y27632 and GF109203X, inhibitors of Rho kinase and protein kinase C, respectively, attenuated EGF-induced contraction, with no diminution of ERK1/2 activity. Although EGF also elevated the activity of EGFR tyrosine kinase in both sham-operated and DOCA-salt hypertensive rats, the expression and the magnitude of activation did not differ between strips. These results strongly suggest that EGF induces contraction by the activation of ERK1/2, which is regulated by the PI3K pathway in the aortic smooth muscle of DOCA-salt hypertensive rats.<br>

収録刊行物

  • Journal of pharmacological sciences  

    Journal of pharmacological sciences 101(2), 135-143, 2006-06-20 

    The Japanese Pharmacological Society

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各種コード

  • NII論文ID(NAID)
    10018237741
  • NII書誌ID(NCID)
    AA11806667
  • 本文言語コード
    ENG
  • 資料種別
    ART
  • ISSN
    13478613
  • NDL 記事登録ID
    7963315
  • NDL 雑誌分類
    ZS51(科学技術--薬学)
  • NDL 請求記号
    Z53-D199
  • データ提供元
    CJP書誌  NDL  J-STAGE 
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