Differential effects of natriuretic peptides on arterial and venous coronary artery bypass conduits

Arterial grafts have patency rates superior to venous grafts in patients undergoing coronary bypass grafting surgery. Natriuretic peptides play a major role in vascular homeostasis. We hypothesized that natriuretic peptides might have different effects on arterial and venous conduits.

Natriuretic peptides are potent vasodilators of the internal mammary artery and radial artery but not the saphenous vein. The relaxation response is mediated through guanylyl cyclase and nitric oxide synthase. These observations may provide additional insight into the mechanisms that account for superior patency of arterial conduits.

The relaxation responses and tissue levels of cyclic guanosine monophosphate (cGMP) after exposure to atrial natriuretic peptide, brain natriuretic peptide, and C-type natriuretic peptide were assessed in segments of internal mammary artery, radial artery, and saphenous vein obtained from the same patients at the time of bypass surgery (n = 12). Natriuretic peptide receptor (NPR) expression was assessed using immunohistochemistry and Western blotting.

Relaxation of the internal mammary artery and radial artery to all the natriuretic peptides were similar, and greater than that of saphenous vein, correlating with increased tissue levels of cGMP in both arterial conduits. Relaxation responses to all three natriuretic peptides were nearly abolished in the presence of LY83583, an inhibitor of guanylyl cyclase. Exposure of the conduits to N(G)-Nitro-L-arginine methyl ester (nitric oxide synthase inhibitor) resulted in a modest but significant blunting of the relaxation responses. Expression of NPR(A), NPR(B) and NPR(C)was strong in the endothelium and vascular smooth muscle layer of the internal mammary artery and radial artery, and was significantly less in saphenous vein. Conclusions: Natriuretic peptides are potent vasodilators of the internal mammary artery and radial artery but not the saphenous vein. The relaxation response is mediated through guanylyl cyclase and nitric oxide synthase. These observations may provide additional insight into the mechanisms that account for superior patency of arterial conduits.