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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

An extract of the first 250 words of the full text is provided, because this article has no abstract.

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 . . . [Full Text of this Article]

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