Difference in endothelium-derived hyperpolarizing factor-mediated hyperpolarization and nitric oxide release between human internal mammary artery and saphenous vein.
BACKGROUND
The greater nitric oxide (NO) release that occurs in the internal mammary artery (IMA) when compared with the saphenous vein (SV) has been suggested by more endothelium-dependent relaxation in the IMA or measured by bioassay; however, no direct measurement of NO- or endothelium-derived hyperpolarizing factor (EDHF)-mediated hyperpolarization has been reported. The present study measured such hyperpolarization, as well as NO release, in these vessels.


RESULTS
IMA (n=46) and SV (n=61) segments taken from patients undergoing coronary surgery were studied in the organ chamber. Hyperpolarization (by intracellular glass microelectrode) and NO release (by NO-sensitive electrode) in response to acetylcholine and bradykinin, with and without incubation with N(G)-nitro-L-arginine, indomethacin, and oxyhemoglobin, were measured. The resting membrane potential of the smooth muscle cells from the IMA (58+/-0.8 mV; n=15) was higher than that in those from the SV (-62+/-0.9 mV; n=23; P:=0.0001). The EDHF-mediated hyperpolarization induced by acetylcholine (10(-5) mol/L: -9.4+/-1.5 mV in IMA, n=10, versus -4. 5+/-1.0 mV in SV, n=17; P:<0.01) and bradykinin (10(-7) mol/L: -10. 9+/-1.5 mV in IMA, n=8, versus -5.1+/-0.5 mV in SV, n=8; P:<0.01) and the basal release of NO (16.8+/-1.6 nmol/L in IMA, n=13, versus 9.9+/-2.8 nmol/L in SV, n=13; P:<0.001) were significantly greater in the IMA than in the SV. The duration of acetylcholine- and bradykinin-induced NO release was longer in the IMA than in the SV.


CONCLUSIONS
The basal release of NO and EDHF-mediated hyperpolarization were significantly greater in the IMA than in the SV. In addition, the duration of the stimulated release of NO was longer in the IMA than in the SV. These differences may contribute to the superior long-term patency of IMA grafts.
Liu
Z G
ZG
Cardiovascular Research Laboratory, Grantham Hospital, University of Hong Kong, Hong Kong, China.
Ge
Z D
ZD
He
G W
GW
D000109:Acetylcholine / Q000494:pharmacology; D001685:Biological Factors / Q000378:metabolism*; D001920:Bradykinin / Q000494:pharmacology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008323:Mammary Arteries / Q000166:cytology / Q000378:metabolism*; D008564:Membrane Potentials / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism*; D009569:Nitric Oxide / Q000096:biosynthesis*; D019335:Nitroarginine / Q000494:pharmacology; D010108:Oxyhemoglobins / Q000494:pharmacology; D012501:Saphenous Vein / Q000166:cytology / Q000378:metabolism*; D014665:Vasodilator Agents / Q000494:pharmacology
D001685:Biological Factors; D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D010108:Oxyhemoglobins; D014665:Vasodilator Agents; C067410:endothelium-dependent hyperpolarization factor; D019335:Nitroarginine; D009569:Nitric Oxide; D000109:Acetylcholine; D001920:Bradykinin; D007213:Indomethacin