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

G. Hajduczok, W. J. Calvo, Robin H Steinhorn, S. F. Gugino, J. A. Russell, S. L. Diamond

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
JournalFASEB Journal
Volume12
Issue number5
StatePublished - Mar 20 1998
Externally publishedYes

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ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

Hajduczok, G., Calvo, W. J., Steinhorn, R. H., Gugino, S. F., Russell, J. A., & Diamond, S. L. (1998). Poststenotic dilatation: Involvement of nitric oxide and altered vascular reactivity in femoral arteries. FASEB Journal, 12(5).