Aging induces muscle-specific impairment of endothelium-dependent dilation in skeletal muscle feed arteries
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 te...
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Published in | Journal of applied physiology (1985) Vol. 93; no. 5; pp. 1685 - 1690 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
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Bethesda, MD
Am Physiological Soc
01.11.2002
American Physiological Society |
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Abstract | 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 |
---|---|
AbstractList | 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. 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. 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 plus or minus 0.04 vs. 0.8 plus or minus 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. 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 |
Author | Woodman, Christopher R Price, Elmer M Laughlin, M. Harold |
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Cites_doi | 10.1016/S0735-1097(96)00394-4 10.1161/01.RES.83.3.279 10.1152/jappl.2001.91.3.1091 10.1093/geronj/42.6.660 10.1161/01.CIR.91.7.1981 10.1152/jappl.1999.87.4.1476 10.1161/01.RES.76.4.536 10.1113/jphysiol.1993.sp019614 10.1152/ajpheart.1999.276.3.H1058 10.1002/clc.4960180810 10.1152/jappl.1999.86.2.441 10.1152/jappl.1998.85.5.1813 10.1172/JCI116092 10.1161/01.RES.79.4.857 10.1161/01.HYP.30.4.817 10.1152/japplphysiol.00032.2002 10.1152/ajpheart.1997.273.4.H1941 10.1161/01.HYP.27.4.849 10.1172/JCI118181 10.1152/ajpheart.1997.273.6.H2575 10.1006/mvre.1994.1057 10.1161/01.RES.79.1.32 10.1161/01.HYP.25.2.194 10.1016/0735-1097(94)90305-0 10.1152/ajpheart.1982.243.2.H296 10.1152/ajpcell.1995.269.6.C1371 10.1152/ajpheart.1995.269.2.H550 |
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Keywords | Senescence Rat Rodentia Striated muscle Soleus muscle Artery Vasodilation Endothelium Vasomotricity Vertebrata Mammalia sodium nitroprusside Blood vessel Nitric oxide superoxide dismutase endothelial nitric oxide synthase Circulatory system Gastrocnemius muscle acetylcholine |
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Snippet | Departments of Veterinary Biomedical Sciences and
Physiology and Dalton Cardiovascular Research Center, University of
Missouri, Columbia, Missouri 65211
We... We tested the hypothesis that aging decreases endothelium-dependent vasodilation in feed arteries perfusing rat skeletal muscle. In addition, we tested the... |
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SubjectTerms | Aging Aging - physiology Animals Arteries - physiology Biological and medical sciences Blood vessels Blood vessels and receptors Endothelium, Vascular - physiology Fundamental and applied biological sciences. Psychology Male Muscle, Skeletal - blood supply Nitric oxide Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type III Rats Rats, Inbred F344 Sodium Superoxide Dismutase - metabolism Superoxide Dismutase-1 Vasodilation - physiology Vertebrates: cardiovascular system |
Title | Aging induces muscle-specific impairment of endothelium-dependent dilation in skeletal muscle feed arteries |
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