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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:1308.)
© 2003 American Heart Association, Inc.

Letters to the Editor

The Resistance of the IMA to Atherosclerosis Might Be Associated With Its Higher eNOS, ACE and ET-A Receptor Immunoreactivity

Anthony Zulli; David L. Hare; Mark Horrigan; Brian F Buxton

Departments of Cardiology (A.Z., D.L.H.) and Cardiac Surgery (A.Z., B.F.B.), University of Melbourne, Austin Health, Heidelberg, and Department of Cardiology (M.H.), Austin Health, Heidelberg, Australia

To the Editor:

Human blood vessels vary in their predisposition to develop atherosclerosis. The internal mammary artery (IMA) is the graft of choice for coronary artery bypass conduit because of its resistance in developing atherosclerosis both before and after bypass grafting.¹ The long-term resistance of the IMA to graft atherosclerosis compared with the saphenous vein (SV) has been attributed, at least in part, to its superior endothelial function.²

Normal endothelial function has been described as the balance between endothelium-derived relaxing factors (such as NO, formed by the conversion of L-arginine to L-citrulline by endothelial NO synthase [eNOS]³) and endothelial-derived contracting factors (such as angiotensin II, formed by the conversion of angiotensin I by angiotensin converting enzyme [ACE] and the oligopeptide endothelin-1 [ET-1], which binds to the ET-A receptor [ET-A]). NO not only stimulates vascular smooth muscle cell relaxation, but it also decreases the maximal binding of ET-1 to ET-A,⁴ and it can inhibit ACE activity.⁵ Therefore, it appears that NO bio-availability may govern endothelium-dependent relaxation, as NO cannot only directly cause smooth muscle cell relaxation, but it can also inhibit vasoconstriction by reducing ACE activity and by decreasing the binding of ET-1 to its receptor.

Therefore, the aim of this study was to quantitate eNOS, ACE, and ET-A in the endothelial cell layer of the internal mammary artery and saphenous vein. ACE, eNOS, and ET-A immunodensity was quantified by using a technique developed in our laboratory.⁶ All results are expressed as relative optical density units per unit volume of endothelium (RODU/µm³), and all data were compared by using a two-tailed Student t test.

Compared with the SV (n=2), the IMA (n=3) has superior endothelial ACE immunodensity (47.7±6.5x10^-6 RODU/µm³ vs 11.6±6.2x10^-6 RODU/µm³, P<0.03), eNOS immunodensity (27.4±2.4x10^-6 RODU/µm³ vs 12.5±6.6x10^-6 RODU/µm³, P<0.05), and ET-A immunodensity (35.3±3.5x10^-6 RODU/µm³ vs 8.9±4.3x10^-6 RODU/µm³, P<0.02). These preliminary results indicate that, although the IMA has higher ACE and ET-A immunodensity, it is associated with an increase in eNOS immunodensity, suggesting that the IMA is a more active vessel.

Thus, we suggest that the activity of a vessel might be a contributing factor to not only its resistance for developing atherosclerosis once used as a bypass conduit but also to its resistance to atherosclerosis in general.

References

1. Tector AJ, Schmahl TM, Janson B, Kallies JR, Johnson G. The internal mammary artery graft: its longevity after coronary bypass. JAMA. 1981; 246: 2181–2183.[Abstract/Free Full Text]

2. Luscher TF, Diederich D, Siebenmann R, Lehmann K, Stulz P, von Segesser L, Yang ZH, Turina M, Gradel E, Weber E, et al. Difference between endothelium-dependent relaxation in arterial and in venous coronary bypass grafts. N Engl J Med. 1988; 319: 462–467.[Abstract]

3. Forstermann U, Schmidt HH, Pollock JS, Sheng H, Mitchell JA, Warner TD, Nakane M, Murad F. Isoforms of nitric oxide synthase: characterization and purification from different cell types. Biochem Pharmacol. 1991; 42: 1849–1857.[CrossRef][Medline] [Order article via Infotrieve]

4. Wiley KE, Davenport AP. Nitric oxide-mediated modulation of the endothelin-1 signalling pathway in the human cardiovascular system. Br J Pharmacol. 2001; 132: 213–220.[CrossRef][Medline] [Order article via Infotrieve]

5. Ackermann A, Fernandez-Alfonso MS, Sanchez de Rojas R, Ortega T, Paul M, Gonzalez C. Modulation of angiotensin-converting enzyme by nitric oxide. Br J Pharmacol. 1998; 124: 291–298.[CrossRef][Medline] [Order article via Infotrieve]

6. Zulli A, Liu JJ. A novel immunohistochemical semiquantitative technique for endothelial constitutive nitric oxide synthase immunoreactivity in rat coronary artery. J Histochem Cytochem. 1998; 46: 257–262.[Abstract/Free Full Text]

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