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 language | English |
|---|---|
| Journal | American Journal of Physiology - Heart and Circulatory Physiology |
| Volume | 267 |
| Issue number | 6 36-6 |
| State | Published - 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)
Cite this
Acute compensation to abrupt occlusion of rat femoral artery is prevented by NO synthase inhibitors. / Unthank, J. L.; Nixon, J. C.; Dalsing, Michael.
In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 267, No. 6 36-6, 1994.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Acute compensation to abrupt occlusion of rat femoral artery is prevented by NO synthase inhibitors
AU - Unthank, J. L.
AU - Nixon, J. C.
AU - Dalsing, Michael
PY - 1994
Y1 - 1994
N2 - 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.
AB - 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.
KW - arterial occlusion
KW - blood flow
KW - collateral arteries
KW - endothelium- dependent vasodilation
KW - endothelium-derived relaxing factor
KW - hindquarter
KW - N(ω)-nitro-L-arginine methyl ester
KW - N(G)-monomethyl-L- arginine
KW - phenylephrine
KW - vascular resistance
UR - http://www.scopus.com/inward/record.url?scp=0028597422&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028597422&partnerID=8YFLogxK
M3 - Article
C2 - 7529001
AN - SCOPUS:0028597422
VL - 267
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0193-1857
IS - 6 36-6
ER -