Background. The extent to which the endothelium regulates radial artery (RA
) contractions is unknown. The goals of this study were to characterize end
othelium-dependent relaxations in the RA, compare these responses with thos
e in the internal mammary artery (IMA), and, subsequently, manipulate nitri
c oxide production in the RA with adenovirus-mediated gene transfer.
Methods. Segments of RA and IMA from 43 patients were studied initially in
organ chambers. Endothelial function was evaluated and gene transfer, was e
xamined.
Results. After precontraction to 80% maximum tension with prostaglandin F-2
alpha, acetylcholine produced lesser relaxations in the RA (21.5% +/- 5.8%
) than in the IMA (66.7% +/- 10.6%); human thrombin and adenosine 5'-diphos
phate yielded similar results. Reduced relaxations in the RA (16.8% +/-: 4.
2%) compared with those IMA (71.6% +/- 11.9%) were noted with calcium ionop
hore. Superfusion bioassay demonstrated a similar baseline release in both
arteries but a reduced stimulated production of vasoactive substances in th
e RA, results confirmed by cyclic guanosine monophosphate level determinati
on. The RA produced less 6-keto-prostaglandin F-1 alpha than the IMA. Light
microscopy demonstrated an intact endothelium in both arteries. Adenovirus
-mediated gene transfer of nitric oxide synthase augmented relaxations of t
he RA to acetylcholine.
Conclusions. Reduced production of endothelium-derived relaxing factors sug
gests diminished endothelial regulation of vascular smooth muscle in the RA
compared with the IMA. This finding may explain, in part, the predispositi
on to vasoconstriction in RA grafts.