Novel Mechanisms of the Antiproliferative Effects of Amlodipine in Vascular Smooth Muscle Cells from Spontaneously Hypertensive Rats

• LAI Yi-Mu

  Second Department of Internal Medicine, Nihon University School of Medicine

• FUKUDA Noboru

  Second Department of Internal Medicine, Nihon University School of Medicine

• SU Jin-Zi

  Second Department of Internal Medicine, Nihon University School of Medicine

• SUZUKI Ryo

  Second Department of Internal Medicine, Nihon University School of Medicine

• IKEDA Yukihiro

  Second Department of Internal Medicine, Nihon University School of Medicine

• TAKAGI Hiroto

  Second Department of Internal Medicine, Nihon University School of Medicine

• TAHIRA Yoshiko

  Second Department of Internal Medicine, Nihon University School of Medicine

• KANMATSUSE Katsuo

  Second Department of Internal Medicine, Nihon University School of Medicine

書誌事項

タイトル別名

• <B>Novel Mechanisms of the Antiproliferative Effects of Amlodipine in Vascular Smooth Muscle Cells from Spontaneously Hypertensive Rats</B>

抄録

The calcium channel blocker amlodipine continues to be of interest due to its potential proven ability to hinder the progression of atherosclerosis and reduce the number of clinical ischemic events. Vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) are useful in the study of atherosclerosis because they show exaggerated growth with production of angiotensin II (Ang II) by conversion to the synthetic phenotype. To clarify mechanisms of the antiproliferative effects of amlodipine, we evaluated effects of the expression of growth factors, the changes in phenotype, and the proliferation of VSMC from SHR. Amlodipine significantly inhibited basal DNA synthesis and proliferation of VSMC from SHR. Amlodipine also inhibited expression of platelet-derived growth factor (PDGF) A-chain, transforming growth factor β1 (TGF-β1) and basic fibroblast growth factor (bFGF) mRNAs in VSMC from SHR. Decreases in levels of PDGF A-chain and bFGF mRNAs in VSMC from SHR were greater with amlodipine than with nifedipine. Amlodipine significantly inhibited expression of the synthetic phenotype markers osteopontin and matrix Gla mRNAs, indicating that it inhibited the exaggerated growth of VSMC from SHR and suppressed the change from the contractile phenotype to the synthetic phenotype. Thus, amlodipine may be a beneficial therapeutic agent for patients with hypertensive vascular diseases. (Hypertens Res 2002; 25: 109-115)

収録刊行物

• Hypertension Research

  Hypertension Research 25 (1), 109-115, 2002

  日本高血圧学会

キーワード

• <B>amlodipine</B>
• <B>vascular smooth muscle cells</B>
• <B>proliferation</B>
• <B>growth factor</B>
• <B>phenotypic modulation</B>

詳細情報

• CRID: 1390282679696822144
• NII論文ID: 10009566959
• NII論文ID: 130004436941
• NII書誌ID: AA10847079
• DOI: 10.1291/hypres.25.109
• COI: 1:CAS:528:DC%2BD38XislCksb8%3D
• ISSN: 13484214
• ISSN: 09169636
• PubMed: 11924715
• Web Site: https://search.jamas.or.jp/link/ui/2002126010
• 本文言語コード: en
• データソース種別:
  • JaLC
  • Crossref
  • PubMed
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可