Atrial Natriuretic Peptide-Induced Release of Cyclic Guanosine Monophosphate by Coronary Bypass Grafts

Background. Superior long-term patency rates of the internal mammary artery (IMA) versus saphenous vein (SV) after coronary artery bypass grafting are well documented. Higher production rates of vasodilating and platelet-inhibiting mediators (prostacyclin and nitric oxide) by the IMA seem to have a major impact on its long-term durability and resistance to coronary artery graft disease. For the right gastroepiploic artery (RGEA) marked release of protective mediators is reported as well. The vasodilating effect of cyclic guanosine monophosphate (cGMP) released after stimulation by atrial natriuretic peptide might serve as another graft protective system. The aim of the present study was to determine cGMP release by IMA, RGEA, and SV after atrial natriuretic peptide challenge. Methods. Samples of human IMA (n = 19), RGEA (n = 7), and SV (n = 18) discarded during coronary artery bypass grafting were stimulated with 10−6 mol/L atrial natriuretic peptide after a resting phase in nutrient me-dium. Release of cGMP was determined by 125-iodide radioimmunoassay. Results. Basal cGMP production rates of the IMA (759.9 ± 277.0 fmol/cm2) and RGEA (739.9 ± 186.0 fmol/cm2) were higher than production rates of SV (281.2 ± 64.0 fmol/cm2). Application of atrial natriuretic peptide led to a statistically significant increase of cGMP release in IMA grafts (1,939.3 ± 778.0 fmol/cm2), whereas RGEA (618.4 ± 141.3 fmol/cm2) and SV (221.7 ± 64.5 fmol/cm2) remained at basal levels (p < 0.05). Conclusions. From these data we conclude that the IMA in comparison with the RGEA and SV produces more extracellular cGMP when stimulated by atrial natriuretic peptide. This effect might support the cGMP-mediated protective properties of nitric oxide and could underline the extraordinary suitability of the IMA as a bypass conduit.