Comparison of nitric oxide release and endothelium-derived hyperpolarizing factor-mediated hyperpolarization between human radial and internal mammary arteries.

Abstract

Arterial grafts for CABG have been used increasingly, and the radial artery (RA) has become a preferable graft, secondary to the internal mammary artery (IMA). In the present study, we investigated and compared NO release and endothelium-derived hyperpolarizing factor (EDHF)-mediated hyperpolarization for IMA and RA. IMA and RA segments taken from CABG patients were placed in an organ chamber. An NO-sensitive electrode (to directly measure NO release) or intracellular glass microelectrode (to measure membrane potential) was used to study NO or EDHF in response to acetylcholine (ACh) and bradykinin (BK) before and after incubation with indomethacin (a cyclooxygenase inhibitor), N(G)-nitro-L-arginine (an NO synthase inhibitor), and oxyhemoglobin (an NO scavenger). The resting membrane potential of the smooth muscle cells of IMA and RA was -58+/-0.84 (n=61) and -61+/-1.3 (n=46) mV, respectively (P=0.03). BK-induced EDHF-mediated hyperpolarization in the IMA was significantly greater than that in RA (BK 10(-)(7) mol/L: -10.9+/-1.5 [n=7] versus -5.8+/-0.9 [n=6] mV, P=0.04). The basal (16.8+/-1.9 versus 11.1+/-1.0 nmol/L, n=12, P=0.02) and stimulated releases of NO in IMA were significantly greater for BK (44.3+/-4.0 versus 25.8+/-3.6 nmol/L, n=8, P=0.004) and lasting longer for ACh (9.5+/-2.0 versus 6.6+/-3.6 minutes, n=12, P=0.03) than those in RA. The basal and stimulated releases of NO and EDHF-mediated hyperpolarization in the IMA are significantly greater than that in the RA. The lower capacity of NO release may contribute to the susceptibility of RA to the perioperative vasospasm and may have an impact on the long-term graft patency.