Acute compensation to abrupt occlusion of rat femoral artery is prevented by NO synthase inhibitors

J. L. Unthank, J. C. Nixon, M. C. Dalsing

Research output: Contribution to journalArticle

23 Scopus citations

Abstract

The hemodynamic significance of endothelium-derived relaxing factor (EDRF)-mediated mechanisms in vascular responses to abrupt rat femoral artery occlusion was investigated. Temporary arterial occlusion was produced before and after inhibition of nitric oxide synthase by N(ω)-nitro-L-arginine methyl ester (L-NAME) or N(G)-monomethyl-L-arginine (L-NMMA). Iliac artery blood flow and arterial pressures proximal and distal to the occlusion were measured. Normal vascular compensation included a return of resistance to preocclusion levels and a rise in distal pressure to a plateau within 5 min postocclusion. After treatment with L-NAME and L-NMMA, postocclusion resistance remained elevated by 53 and 36%, respectively. Collateral dilation after occlusion, as indicated by the rise in distal pressure, was prevented by L-NAME but not L-NMMA. Increases in adrenergic tone and mean arterial pressure by phenylephrine did not prevent compensation, suggesting the effects of L-NAME and L-NMMA did not result from elevated sympathetic activation or pressure. The results are consistent with the hypothesis that the stimulated release of endothelium-derived relaxing factor mediates the acute vascular compensation to abrupt arterial occlusion.

Original languageEnglish (US)
Pages (from-to)H2523-H2530
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume267
Issue number6 36-6
DOIs
StatePublished - Jan 1 1994

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Keywords

  • arterial occlusion
  • blood flow
  • collateral arteries
  • endothelium- dependent vasodilation
  • endothelium-derived relaxing factor
  • hindquarter
  • N(ω)-nitro-L-arginine methyl ester
  • N(G)-monomethyl-L- arginine
  • phenylephrine
  • vascular resistance

ASJC Scopus subject areas

  • Physiology
  • Agricultural and Biological Sciences(all)

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