Nitric oxide and endothelium-derived hyperpolarizing factor in human arteries and veins

We have investigated and compared nitric oxide (NO) release and endothelium-derived hyperpolarizing factor (EDHF)-mediated hyperpolarization in the human internal mammary artery (IMA), radial artery (RA), saphenous vein (SV), and coronary artery.

Vessel segments taken from coronary artery bypass grafting or heart transplantation patients were placed in an organ chamber. NO-sensitive electrode or intracellular glass microelectrode was used to study NO or EDHF in response to acetylcholine (ACh) and bradykinin (BK).

The resting membrane potential of the smooth muscle cells of IMA, RA, and SV was -58 +/- 0.84 (n = 61), -61 +/- 1.3 mV (n = 46, p = 0.03), and -62 +/- 0.9 mV (n = 23, p = 0.0001) respectively. BK- (10(-7) M) induced EDHF-mediated hyperpolarization (-10.9 +/- 1.5 mV, n = 7) in the IMA was significantly greater than that in RA (-5.8 +/- 0.9 mV, n = 6, p = 0.04) and SV (-5.1 +/- 0.5 mV, n = 8, p < 0.01). The basal release of NO in IMA (16.8 +/- 1.9 nM) was significantly higher than that in RA (11.1 +/- 1.0 nM, n = 12, p = 0.02) and in SV (9.9 +/- 2.8 nM, n = 13, p < 0.001). The stimulated release of NO to BK in IMA was significantly greater than that in RA (44.3 +/- 4.0 vs 25.8 +/- 3.6 nM, n = 8, p = 0.004). The duration of NO release was longer in IMA than in RA or in SV.

The basal and stimulated release of NO and EDHF-mediated hyperpolarization in the IMA are significantly greater than that in the RA and SV. EDHF exists in all these human vessels. This study reveals the differences among human vessels regarding the endothelial function that have implications in vasospasm, coronary protection, or long-term graft patency.