Effects of Valsartan on Angiotensin II-Induced Migration of Human Coronary Artery Smooth Muscle Cells.

• KOHNO Masakazu

  Second Department of Internal Medicine, School of Medicine, Kagawa Medical University

• OHMORI Koji

  Second Department of Internal Medicine, School of Medicine, Kagawa Medical University

• NOZAKI Shiro

  Second Department of Internal Medicine, School of Medicine, Kagawa Medical University

• MIZUSHIGE Katsufumi

  Second Department of Internal Medicine, School of Medicine, Kagawa Medical University

• YASUNARI Kenichi

  First Department of Internal Medicine, Osaka City University Medical School

• KANO Hiroaki

  First Department of Internal Medicine, Osaka City University Medical School

• MINAMI Mieko

  First Department of Internal Medicine, Osaka City University Medical School

• YOSHIKAWA Junichi

  First Department of Internal Medicine, Osaka City University Medical School

Abstract

The migration as well as proliferation of coronary artery medial smooth muscle cells (SMC) into the intima is proposed to be an important process of intimal thickening in coronary atherosclerosis. In the current study, we examined the effects of the angiotensin type 1 receptor antagonist valsartan on angiotensin II (Ang II)-induced migration of cultured human coronary artery SMC using Boyden's chamber methods. Ang II significantly stimulated human coronary artery SMC migration in a concentration-dependent manner between 10^-6 and 10^-8mol/l when cells of passage 4 to 6 were used. However, the migration response to Ang II was moderately decreased in cells of passage 10 to 12, and was markedly decreased in cells of passage 15 to 17, compared to that of passage 4 to 6. Ang II-induced migration was blocked by the Ang II type 1 (AT₁) receptor antagonist valsartan in a concentration-dependent manner. By contrast, the Ang II type 2 (AT₂) receptor antagonist PD 123319 did not affect Ang II-induced migration. Ang II modestly increased the cell number of human coronary artery SMC after a 24-h incubation. This increase in cell numbers was also clearly blocked by valsartan, but not by PD 123319. These results indicate that Ang II stimulates migration as well as proliferation via AT₁ receptors in human coronary artery SMC when cells of passage 4 to 6 are used. Valsartan may prevent the progression of coronary atherosclerosis through an inhibition of Ang II-induced migration and proliferation in these cells, although in vivo evidence is lacking. (Hypertens Res 2000; 23: 677-681)

Journal

• Hypertension Research

  Hypertension Research 23 (6), 677-681, 2000

  The Japanese Society of Hypertension

Keywords

• angiotensin II
• angiotensin receptor antagonist
• migration
• smooth muscle cells

Details

• CRID: 1390001204718794624
• NII Article ID: 130003456486
• NII Article ID: 30034931577
• NII Article ID: 10008741229
• NII Book ID: AA10847079
• DOI: 10.1291/hypres.23.677
• COI: 1:CAS:528:DC%2BD3cXptVags74%3D
• ISSN: 13484214
• ISSN: 09169636
• ISSN: http://id.crossref.org/issn/09169636
• PubMed: 11131281
• Web Site: https://search.jamas.or.jp/link/ui/2001139319
• Text Lang: en
• Data Source:
  • JaLC
  • Crossref
  • PubMed
  • CiNii Articles
• Abstract License Flag: Disallowed