Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Vascular Medicine
This Article
Right arrow Full Text (PDF)
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Tang, L.
Right arrow Articles by Taylor, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tang, L.
Right arrow Articles by Taylor, R.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

ACE inhibition and fibroblast growth factor in cultured human vascular smooth muscle

Lilong Tang

Department of Cardiology, Royal Perth Hospital, Perth

Katrin Both

Department of Medicine, The University of Western Australia and the West Australian Heart Research Institute, Western Australia, Australia

Roger Taylor

Department of Cardiology, Royal Perth Hospital, Perth, Department of Medicine, The University of Western Australia and the West Australian Heart Research Institute, Western Australia, Australia

The effects of the angiotensin converting enzyme (ACE) inhibitor, enalaprilat, and basic fibroblast growth factor (bFGF) on DNA synthesis and expression of ACE mRNA were examined in human vascular smooth muscle cells cultured from saphenous vein and internal mammary artery.

DNA synthesis was estimated using 3H-thymidine uptake, and ACE mRNA was estimated by rt-PCR. Enalaprilat (0.125 mg/ml, 48 h) decreased 3H-thymidine uptake to 66 - 12% (SE) of the control without enalaprilat (p, 0.05). Basic FGF (10 ng/ml, 24 h) increased uptake by 41 - 12% (p, 0.05) while enalaprilat pretreatment (24 h) decreased uptake to 56 - 12% of this augmented value (p, 0.025). Basic FGF increased ACE mRNA, a process that was time dependent with an approximately 50% increase after 24 h exposure. Pre-exposure to enalaprilat (24 h) before bFGF reduced ACE mRNA to approximately 50% of that found in the presence of bFGF alone.

The results indicate that ACE mRNA is present in human vascular smooth muscle cells and that exposure to an ACE inhibitor reduces DNA synthesis. Basic FGF stimulates DNA synthesis and ACE mRNA expression, and both of these effects are reduced by an ACE inhibitor. The results are consistent with the effects of bFGF being exerted through, or alternatively in concert with, angiotensin II. Further, they suggest that ACE inhibition can reduce the activity of the renin-angiotensin system by inhibiting the production of ACE, or at least the expression of ACE mRNA, in addition to producing enzyme inhibition at the ACE level.

Key Words: angiotensin converting enzyme inhibition • enalaprilat • fibroblast growth factor • human smooth muscle • vascular smooth muscle

Vascular Medicine, Vol. 4, No. 3, 129-134 (1999)
DOI: 10.1177/1358836X9900400302


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?