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Departments of Veterinary Biomedical Sciences and Physiology and Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211
We tested the hypothesis that aging
decreases endothelium-dependent vasodilation in feed arteries perfusing
rat skeletal muscle. In addition, we tested the hypothesis that
attenuated vasodilator responses are associated with decreased
endothelial nitric oxide synthase (eNOS) and superoxide dismutase-1
(SOD-1) expression. Soleus feed arteries (SFA) and gastrocnemius feed
arteries (GFA) were isolated from young (4 mo) and old (24 mo) male
Fischer 344 rats. Feed arteries from the right hindlimb were cannulated
with two glass micropipettes for examination of endothelium-dependent [acetylcholine (ACh)] and endothelium-independent [adenosine
(Ado) or sodium nitroprusside (SNP)] vasodilator function. Feed
arteries from the left hindlimb were frozen and used to assess eNOS and SOD-1 protein and mRNA expression. In SFA, endothelium-dependent dilation to ACh was reduced in old rats (0.9 ± 0.04 vs. 0.8 ± 0.03), whereas dilator responses to Ado and SNP were similar in SFA
of young and old rats. In GFA, vasodilator responses to ACh, Ado, and SNP were not altered by age. eNOS and SOD-1 protein expression declined with age in SFA (
71 and 54%, respectively) but not in
GFA. eNOS and SOD-1 mRNA expression were not altered by age in SFA or
GFA. Collectively, these data indicate aging induces muscle-specific
impairment of endothelium-dependent vascular function in SFA.
endothelial nitric oxide synthase; superoxide dismutase; nitric oxide; acetylcholine; sodium nitroprusside
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