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Ann Thorac Surg 1998;65:1624
© 1998 The Society of Thoracic Surgeons


Original articles: cardiovascular

Invited commentary

Amer Chaikhouni, MDa

a PO Box 8795, Aleppo, Syria


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The higher production of cyclic guanosine monophosphate by arterial conduits, particularly the internal mammary artery, may play a role in the well-documented improved patency of these conduits. Other factors, such as wall thickness ratio, intact adventitia, and production of prostacyclin and nitric oxide may also be of major importance. The difference in response to atrial natriuretic peptide (ANP) between internal mammary artery, right gastroepiploic artery, and saphenous vein in this study by Bonatti and associates may be a result of differences in available receptors in these vessels. Most physiologic actions of ANP appear to be mediated by attachment to a specific receptor on the cell membrane, with subsequent activation of guanylyl cyclase and the formation of cyclic guanosine monophosphate. It is difficult to confirm whether the dose of ANP used in this study is indeed of true significance in physiologic conditions. Atrial natriuretic peptide is well known to have variable response when used in pharmacologic doses in vitro, in animals, and in human volunteers. However, this study focuses attention on the potential use of ANP, and probably even more so for ANP receptor (ant)agonists, in the treatment of hypertension, congestive heart failure, renal failure, and vascular proliferative diseases. Morishita and colleagues [1] demonstrated that ANP can inhibit endothelial and vascular smooth muscle growth, and in vivo gene transfer of ANP may be a new approach to treat vasoconstrictive and pathologic growth of vascular smooth muscle. Can this be a potential solution to the difficult restenosis problem after percutaneous transluminal coronary angioplasty?


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  1. Morishita R., Gibbons G.H., Pratt R.E., et al. Autocrine and paracrine effects of atrial natriuretic peptide gene transfer on vascular smooth muscle and endothelial cellular growth. J Clin Invest 1994;94:824-829.




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