Poststenotic dilatation: Involvement of nitric oxide and altered vascular reactivity in femoral arteries

We hypothesized that nitric oxide (NO) elicited by high fluid shear stress acting on the endothelium in the throat of the stenosis and/or at the focal site of flow reattachment may be an important mediator of poststenotic dilatation (PSD). Femoral arteries of 5 adult male New Zealand white rabbits were stenosed bilaterally to achieve a diameter reduction of 74±5% (n=10). At the time of stenosis, the adventitia of a the stenosed arteries was coated with 1 mM of NG-nitro-L-arginine methyl ester (LNAME) in 22% (w/v) pluronic gel, while the contralateral vessel was coated with gel without LNAME. In stenosed femoral arteries that were treated with gel only, a maximum PSD of 29±8% (n=5) was observed in polymer casts at 3 days. In contrast, the vessels treated with LNAME exhibited a maximum PSD of only 4±5% (n=5). Vascular rings from stenosed proximal (n=9) and distal (n=8) segments, as well as from the contralateral sham operated (n=6) arteries were also studied from 3 animals in tissue baths. Endothelium-dependent relaxations to acetylcholine in arteries contracted submaximally by phenylephrine were greater in the distal (PSD) segments (p<0.05) as compared with control or the proximal segments. We conclude that wall shear stresses within the stenosis and/or at the focal site of flow reattachment elicit endothelial production of NO to cause PSD and enhances receptor stimulated release of NO.