(Circulation. 1999;100:1223-1229.)
© 1999 American Heart Association, Inc.
Basic Science Reports |
Angiotensin II Induces Vascular Cell Adhesion Molecule-1 Expression In Rat Vasculature
A Potential Link Between the Renin-Angiotensin System and Atherosclerosis
From the Division of Cardiology (P.E.T., X.-L.C., R.W.A., D.G.H., R.M.M.), Department of Medicine, Emory University School of Medicine, Atlanta, Ga; AtheroGenics Inc. (C.L.S., C.P.H., R.M.M.), Norcross, Ga; and Division of Cardiology (J.B.L.), Rigshospitalet, Copenhagen, Denmark.
Correspondence to Russell M. Medford MD, PhD, AtheroGenics Inc., 8995 Westside Parkway, Alpharetta, GA 30004. E-mail rmedford{at}atherogenics.com
Background—Cardiovascular ischemic events may occur more frequently in hypertensive patients with activated renin-angiotensin systems. We tested the hypothesis that angiotensin II (Ang II) may contribute to atherosclerosis by increasing expression of vascular inflammatory genes such as vascular cell adhesion molecule-1 (VCAM-1).
Methods and Results—Rats infused with norepinephrine
or Ang II for 6 days developed similar hypertensive responses, but only
Ang II-treated rats exhibited significant increases in aortic VCAM-1
protein and mRNA expression. Oral losartan treatment (50
mg · kg-1 · d-1) inhibited Ang
II-induced hypertension and aortic VCAM-1 mRNA expression. Ang II
treatment significantly increased VCAM-1 mRNA expression in cultured
rat aortic smooth muscle cells (RASMCs). Ang II also induced nuclear
NF-
B-like binding activity and transactivated an
NF-B–driven VCAM-1 promoter. Losartan and proteasome
inhibitors blocked Ang II-induced NF-B activation and
VCAM-1 mRNA accumulation. IB-
overexpression in RASMCs inhibited
Ang II-induced VCAM-1 promoter transactivation.
Conclusions—Ang II may contribute to atherogenesis by activation
of VCAM-1 through proteasome dependent, NF-B-like transcriptional
mechanisms.
Key Words: angiotensin • hypertension • VCAM-1 • NF-B
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