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Differential effects of natriuretic peptides on arterial and venous coronary artery bypass conduits
Hao G Nguyen1, Amit Korach, Chey Collura
1Department of Cardiothoracic Surgery, Boston Medical Center, Boston, Massachusetts, USA.
Insights
Natriuretic peptides strongly relax arterial grafts, unlike venous grafts, via guanylyl cyclase and nitric oxide. This explains why arterial conduits offer superior patency in coronary bypass surgery.
Area of Science:
- Cardiovascular Research
- Vascular Biology
- Pharmacology
Background:
- Arterial grafts demonstrate superior patency rates compared to venous grafts in coronary bypass grafting (CABG) surgery.
- Natriuretic peptides are key regulators of vascular homeostasis.
- The differential effects of natriuretic peptides on arterial versus venous conduits remain to be elucidated.
Purpose of the Study:
- To investigate the differential effects of natriuretic peptides on arterial and venous conduits used in CABG.
- To explore the underlying mechanisms, including cyclic guanosine monophosphate (cGMP) and natriuretic peptide receptor (NPR) expression, mediating these effects.
Main Methods:
- Segments of internal mammary artery, radial artery, and saphenous vein from CABG patients (n=12) were used.
- Relaxation responses to atrial natriuretic peptide, brain natriuretic peptide, and C-type natriuretic peptide were measured.
- Tissue cGMP levels, NPR expression (immunohistochemistry, Western blotting), and effects of guanylyl cyclase and nitric oxide synthase inhibitors were assessed.
Main Results:
- Internal mammary artery and radial artery showed greater relaxation to natriuretic peptides than saphenous vein, with higher cGMP levels.
- Relaxation was significantly reduced by guanylyl cyclase inhibitor LY83583 and modestly by nitric oxide synthase inhibitor N(G)-Nitro-L-arginine methyl ester.
- NPR(A), NPR(B), and NPR(C) expression was significantly higher in arterial conduits compared to saphenous vein.
Conclusions:
- Natriuretic peptides act as potent vasodilators for arterial conduits (internal mammary artery, radial artery) but not for venous conduits (saphenous vein).
- The vasodilatory effects are mediated via the guanylyl cyclase and nitric oxide synthase pathways.
- These findings offer insights into the superior patency of arterial grafts in coronary bypass surgery.
Background:
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.
Methods:
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.
Results:
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.
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