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(Circulation. 1996;94:2756-2767.)
© 1996 American Heart Association, Inc.

Articles

Increased Accumulation of Tissue ACE in Human Atherosclerotic Coronary Artery Disease

Frank Diet, MD; Richard E. Pratt, PhD; Gerald J. Berry, MD; Naoko Momose, MD; Gary H. Gibbons, MD; Victor J. Dzau, MD

the Division of Cardiovascular Medicine, Falk Cardiovascular Center, Stanford University Medical Center, Stanford, Calif.

Correspondence to Richard E. Pratt, PhD, Dept of Medicine, Brigham & Women's Hospital, Thorn-12, 75 Francis St, Boston, MA 02115.

Background Angiotensin may play a pathophysiological role in experimental and human cardiovascular disease. Clinical studies have shown that ACE inhibitors reduce mortality, recurrent myocardial infarction, and ischemic events in patients with left ventricular dysfunction. Animal studies suggest that tissue ACE, particularly within blood vessels, may be an important target.

Methods and Results To study tissue ACE in human coronary artery disease and to identify potential mechanisms of ACE inhibitor action, we examined ACE expression immunohistochemically in nonatherosclerotic and diseased human coronary arteries. In nonatherosclerotic arteries, ACE immunoreactivity was found in luminal and adventitial vasa vasorum endothelium. In early- and intermediate-stage atherosclerotic lesions, ACE was detected prominently in regions of fat-laden macrophages and in association with T lymphocytes. In advanced lesions, ACE immunoreactivity was also localized to the endothelium of the microvasculature throughout the plaques. Immunoreactive angiotensin II was also detected in these areas. ACE expression in macrophages was further examined by in vitro experiments with a monocytoid cell line. ACE activity was induced threefold after differentiation of the cells into macrophages and was further increased after stimulation with acetylated LDL.

Conclusions These observations demonstrate that significant sources of tissue ACE in human atherosclerotic plaques are regions of inflammatory cells, especially areas of clustered macrophages as well as microvessel endothelial cells. These results suggest that ACE accumulation within the plaque may contribute to an increased production of local angiotensin that may participate in the pathobiology of coronary artery disease. Plaque ACE probably is an important target of drug action.

Key Words: angiotensin • vasculature • endothelium • immunohistochemistry • lipoproteins

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				A. Warnholtz, G. Nickenig, E. Schulz, R. Macharzina, J. H. Brasen, M. Skatchkov, T. Heitzer, J. P. Stasch, K. K. Griendling, D. G. Harrison, et al. Increased NADH-Oxidase–Mediated Superoxide Production in the Early Stages of Atherosclerosis : Evidence for Involvement of the Renin-Angiotensin System Circulation, April 20, 1999; 99(15): 2027 - 2033. [Abstract] [Full Text] [PDF]

				Y. Yanagitani, H. Rakugi, A. Okamura, K. Moriguchi, S. Takiuchi, M. Ohishi, K. Suzuki, J. Higaki, and T. Ogihara Angiotensin II Type 1 Receptor–Mediated Peroxide Production in Human Macrophages Hypertension, January 1, 1999; 33(1): 335 - 339. [Abstract] [Full Text] [PDF]

				M. A. Hernandez-Presa, C. Bustos, M. Ortego, J. Tunon, L. Ortega, and J. Egido ACE Inhibitor Quinapril Reduces the Arterial Expression of NF-{kappa}B-Dependent Proinflammatory Factors but not of Collagen I in a Rabbit Model of Atherosclerosis Am. J. Pathol., December 1, 1998; 153(6): 1825 - 1837. [Abstract] [Full Text] [PDF]

				H. Tomita, K. Egashira, M. Kubo-Inoue, M. Usui, M. Koyanagi, H. Shimokawa, M. Takeya, T. Yoshimura, and A. Takeshita Inhibition of NO Synthesis Induces Inflammatory Changes and Monocyte Chemoattractant Protein-1 Expression in Rat Hearts and Vessels Arterioscler Thromb Vasc Biol, September 1, 1998; 18(9): 1456 - 1464. [Abstract] [Full Text] [PDF]

				B. Yang, D. Li, M I. Phillips, P. Mehta, and J. L Mehta Myocardial angiotensin II receptor expression and ischemia-reperfusion injury Vascular Medicine, May 1, 1998; 3(2): 121 - 130. [Abstract] [PDF]

				M. Pfeifer, G. Bruckschlegel, S. R Holmer, M. Paul, A.J.G. Riegger, and H. Schunkert Reciprocal regulation of pulmonary and cardiac angiotensin-converting enzyme in rats with severe left ventricular hypertrophy Cardiovasc Res, April 1, 1998; 38(1): 125 - 132. [Abstract] [Full Text] [PDF]

				A. Lucas, E. Dai, L.-Y. Liu, and P. N Nation Atherosclerosis in Marek's disease virus infected hypercholesterolemic roosters is reduced by HMGCoA reductase and ACE inhibitor therapy Cardiovasc Res, April 1, 1998; 38(1): 237 - 246. [Abstract] [Full Text] [PDF]

				R. W. Nesto and S. Zarich Acute Myocardial Infarction in Diabetes Mellitus : Lessons Learned From ACE Inhibition Circulation, January 13, 1998; 97(1): 12 - 15. [Full Text] [PDF]

				M. Kubo-Inoue, K. Egashira, M. Usui, M. Takemoto, K. Ohtani, M. Katoh, H. Shimokawa, and A. Takeshita Long-term inhibition of nitric oxide synthesis increases arterial thrombogenecity in rat carotid artery Am J Physiol Heart Circ Physiol, April 1, 2002; 282(4): H1478 - H1484. [Abstract] [Full Text] [PDF]

				S. Rajagopalan, D. Duquaine, S. King, B. Pitt, and P. Patel Mineralocorticoid Receptor Antagonism in Experimental Atherosclerosis Circulation, May 7, 2002; 105(18): 2212 - 2216. [Abstract] [Full Text] [PDF]