Hindlimb unweighting alters endothelium-dependent vasodilation and ecNOS expression in soleus arterioles

Departments of Physiology and Veterinary Biomedical Sciences and Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211 The purpose of this study was to test the hypothesis that endothelium-dependent dilation is impaired in soleus resistance arteries from hindlimb-un...

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Published inJournal of applied physiology (1985) Vol. 89; no. 4; pp. 1483 - 1490
Main Authors Schrage, William G, Woodman, Christopher R, Laughlin, M. Harold
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Published Bethesda, MD Am Physiological Soc 01.10.2000
American Physiological Society
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Abstract Departments of Physiology and Veterinary Biomedical Sciences and Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211 The purpose of this study was to test the hypothesis that endothelium-dependent dilation is impaired in soleus resistance arteries from hindlimb-unweighted (HLU) rats. Male Sprague-Dawley rats (300-350 g) were exposed to HLU ( n  = 14) or weight-bearing control (Con, n  = 14) conditions for 14 days. After the 14-day treatment period, soleus first-order (1A) arterioles were isolated and cannulated with micropipettes to assess vasodilator responses to an endothelium-dependent dilator, ACh (10 9 -10 4 M), and an endothelium-independent dilator, sodium nitroprusside (SNP, 10 9 -10 4 M). Arterioles from HLU rats were smaller than Con arterioles (maximal passive diameter = 140 ± 4 and 121 ± 4 µm in Con and HLU, respectively) but developed similar spontaneous myogenic tone (43 ± 3 and 45 ± 3% in Con and HLU, respectively). Arteries from Con and HLU rats dilated in response to increasing doses of ACh, but dilation was impaired in arterioles from HLU rats ( P  = 0.03), as was maximal dilation to ACh (85 ± 4 and 65 ± 4% possible dilation in Con and HLU, respectively). Inhibition of nitric oxide (NO) synthase (NOS) with N -nitro- L -arginine (300 µM) reduced ACh dilation by ~40% in arterioles from Con rats and eliminated dilation in arterioles from HLU rats. The cyclooxygenase inhibitor indomethacin (50 µM) did not significantly alter dilation to ACh in either group. Treatment with N -nitro- L -arginine + indomethacin eliminated all ACh dilation in Con and HLU rats. Dilation to sodium nitroprusside was not different between groups ( P  = 0.98). To determine whether HLU decreased expression of endothelial cell NOS (ecNOS), mRNA and protein levels were measured in single arterioles with RT-PCR and immunoblot analysis. The ecNOS mRNA and protein expression was significantly lower in arterioles from HLU rats than in Con arterioles (20 and 65%, respectively). Collectively, these data indicate that HLU impairs ACh dilation in soleus 1A arterioles, in part because of alterations in the NO pathway. skeletal muscle; microcirculation; acetylcholine; microgravity; physical inactivity; indomethacin; N -nitro- L -arginine
AbstractList The purpose of this study was to test the hypothesis that endothelium-dependent dilation is impaired in soleus resistance arteries from hindlimb-unweighted (HLU) rats. Male Sprague-Dawley rats (300-350 g) were exposed to HLU (n = 14) or weight-bearing control (Con, n = 14) conditions for 14 days. After the 14-day treatment period, soleus first-order (1A) arterioles were isolated and cannulated with micropipettes to assess vasodilator responses to an endothelium-dependent dilator, ACh (10(-9)-10(-4) M), and an endothelium-independent dilator, sodium nitroprusside (SNP, 10(-9)-10(-4) M). Arterioles from HLU rats were smaller than Con arterioles (maximal passive diameter = 140 +/- 4 and 121 +/- 4 microm in Con and HLU, respectively) but developed similar spontaneous myogenic tone (43 +/- 3 and 45 +/- 3% in Con and HLU, respectively). Arteries from Con and HLU rats dilated in response to increasing doses of ACh, but dilation was impaired in arterioles from HLU rats (P = 0.03), as was maximal dilation to ACh (85 +/- 4 and 65 +/- 4% possible dilation in Con and HLU, respectively). Inhibition of nitric oxide (NO) synthase (NOS) with N(omega)-nitro-L-arginine (300 microM) reduced ACh dilation by approximately 40% in arterioles from Con rats and eliminated dilation in arterioles from HLU rats. The cyclooxygenase inhibitor indomethacin (50 microM) did not significantly alter dilation to ACh in either group. Treatment with N(omega)-nitro-L-arginine + indomethacin eliminated all ACh dilation in Con and HLU rats. Dilation to sodium nitroprusside was not different between groups (P = 0.98). To determine whether HLU decreased expression of endothelial cell NOS (ecNOS), mRNA and protein levels were measured in single arterioles with RT-PCR and immunoblot analysis. The ecNOS mRNA and protein expression was significantly lower in arterioles from HLU rats than in Con arterioles (20 and 65%, respectively). Collectively, these data indicate that HLU impairs ACh dilation in soleus 1A arterioles, in part because of alterations in the NO pathway.
The purpose of this study was to test the hypothesis that endothelium-dependent dilation is impaired in soleus resistance arteries from hindlimb-unweighted (HLU) rats. Male Sprague-Dawley rats (300-350 g) were exposed to HLU (n = 14) or weight-bearing control (Con, n = 14) conditions for 14 days. After the 14-day treatment period, soleus first-order (1A) arterioles were isolated and cannulated with micropipettes to assess vasodilator responses to an endothelium-dependent dilator, ACh (10 exp -9 to 10 exp -4 M), and an endotheliumindependent dilator, sodium nitroprusside (SNP, 10 exp -9 to 10 exp -4 M). Arterioles from HLU rats were smaller than Con arterioles (maximal passive diameter = 140 +/- 4 and 121 +/- 4 microns in Con and HLU, respectively) but developed similar spontaneous myogenic tone (43 +/- 3 and 45 +/- 3 percent in Con and HLU, respectively). Arteries from Con and HLU rats dilated in response to increasing doses of ACh, but dilation was impaired in arterioles from HLU rats (P = 0.03), as was maximal dilation to ACh (85 +/- 4 and 65 +/- 4 percent possible dilation in Con and HLU, respectively). Inhibition of nitric oxide (NO) synthase (NOS) with N(sup omega)-nitro-L-arginine (300 micro-M) reduced ACh dilation by approximately 40 percent in arterioles from Con rats and eliminated dilation in arterioles from HLU rats. The cyclooxygenase inhibitor indomethacin (50 micro-M) did not significantly alter dilation to ACh in either group. Treatment with N(sup omega)-nitro-L-arginine + indomethacin eliminated all ACh dilation in Con and HLU rats. Dilation to sodium nitroprusside was not different between groups (P = 0.98). To determine whether HLU decreased expression of endothelial cell NOS (ecNOS), mRNA and protein levels were measured in single arterioles with RT-PCR and immunoblot analysis. The ecNOS mRNA and protein expression was significantly lower in arterioles from HLU rats than in Con arterioles (20 and 65 percent, respectively). Collectively, these data indicate that HLU impairs ACh dilation in soleus 1A arterioles, in part because of alterations in the NO pathway. (Author)
The purpose of this study was to test the hypothesis that endothelium-dependent dilation is impaired in soleus resistance arteries from hindlimb-unweighted (HLU) rats. Male Sprague-Dawley rats (300-350 g) were exposed to HLU (n = 14) or weight-bearing control (Con, n = 14) conditions for 14 days.
Departments of Physiology and Veterinary Biomedical Sciences and Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211 The purpose of this study was to test the hypothesis that endothelium-dependent dilation is impaired in soleus resistance arteries from hindlimb-unweighted (HLU) rats. Male Sprague-Dawley rats (300-350 g) were exposed to HLU ( n  = 14) or weight-bearing control (Con, n  = 14) conditions for 14 days. After the 14-day treatment period, soleus first-order (1A) arterioles were isolated and cannulated with micropipettes to assess vasodilator responses to an endothelium-dependent dilator, ACh (10 9 -10 4 M), and an endothelium-independent dilator, sodium nitroprusside (SNP, 10 9 -10 4 M). Arterioles from HLU rats were smaller than Con arterioles (maximal passive diameter = 140 ± 4 and 121 ± 4 µm in Con and HLU, respectively) but developed similar spontaneous myogenic tone (43 ± 3 and 45 ± 3% in Con and HLU, respectively). Arteries from Con and HLU rats dilated in response to increasing doses of ACh, but dilation was impaired in arterioles from HLU rats ( P  = 0.03), as was maximal dilation to ACh (85 ± 4 and 65 ± 4% possible dilation in Con and HLU, respectively). Inhibition of nitric oxide (NO) synthase (NOS) with N -nitro- L -arginine (300 µM) reduced ACh dilation by ~40% in arterioles from Con rats and eliminated dilation in arterioles from HLU rats. The cyclooxygenase inhibitor indomethacin (50 µM) did not significantly alter dilation to ACh in either group. Treatment with N -nitro- L -arginine + indomethacin eliminated all ACh dilation in Con and HLU rats. Dilation to sodium nitroprusside was not different between groups ( P  = 0.98). To determine whether HLU decreased expression of endothelial cell NOS (ecNOS), mRNA and protein levels were measured in single arterioles with RT-PCR and immunoblot analysis. The ecNOS mRNA and protein expression was significantly lower in arterioles from HLU rats than in Con arterioles (20 and 65%, respectively). Collectively, these data indicate that HLU impairs ACh dilation in soleus 1A arterioles, in part because of alterations in the NO pathway. skeletal muscle; microcirculation; acetylcholine; microgravity; physical inactivity; indomethacin; N -nitro- L -arginine
The purpose of this study was to test the hypothesis that endothelium-dependent dilation is impaired in soleus resistance arteries from hindlimb-unweighted (HLU) rats. Male Sprague-Dawley rats (300–350 g) were exposed to HLU ( n = 14) or weight-bearing control (Con, n = 14) conditions for 14 days. After the 14-day treatment period, soleus first-order (1A) arterioles were isolated and cannulated with micropipettes to assess vasodilator responses to an endothelium-dependent dilator, ACh (10 −9 –10 −4 M), and an endothelium-independent dilator, sodium nitroprusside (SNP, 10 −9 –10 −4 M). Arterioles from HLU rats were smaller than Con arterioles (maximal passive diameter = 140 ± 4 and 121 ± 4 μm in Con and HLU, respectively) but developed similar spontaneous myogenic tone (43 ± 3 and 45 ± 3% in Con and HLU, respectively). Arteries from Con and HLU rats dilated in response to increasing doses of ACh, but dilation was impaired in arterioles from HLU rats ( P = 0.03), as was maximal dilation to ACh (85 ± 4 and 65 ± 4% possible dilation in Con and HLU, respectively). Inhibition of nitric oxide (NO) synthase (NOS) with N ω -nitro-l-arginine (300 μM) reduced ACh dilation by ∼40% in arterioles from Con rats and eliminated dilation in arterioles from HLU rats. The cyclooxygenase inhibitor indomethacin (50 μM) did not significantly alter dilation to ACh in either group. Treatment with N ω -nitro-l-arginine + indomethacin eliminated all ACh dilation in Con and HLU rats. Dilation to sodium nitroprusside was not different between groups ( P = 0.98). To determine whether HLU decreased expression of endothelial cell NOS (ecNOS), mRNA and protein levels were measured in single arterioles with RT-PCR and immunoblot analysis. The ecNOS mRNA and protein expression was significantly lower in arterioles from HLU rats than in Con arterioles (20 and 65%, respectively). Collectively, these data indicate that HLU impairs ACh dilation in soleus 1A arterioles, in part because of alterations in the NO pathway.
Author Woodman, Christopher R
Schrage, William G
Laughlin, M. Harold
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Cites_doi 10.1161/01.CIR.99.22.2951
10.1152/ajpheart.2000.278.1.H233
10.1152/jappl.1999.87.4.1476
10.2307/1307797
10.1161/01.RES.22.1.83
10.1152/jappl.1994.76.5.2241
10.1152/jappl.1987.63.2.558
10.1152/jappl.1995.78.6.2079
10.1152/jappl.1995.79.5.1762
10.1152/jappl.1999.86.4.1178
10.1152/jappl.1992.72.6.2210
10.1152/jappl.1997.82.5.1488
10.1016/0076-6879(69)13005-0
10.1152/jappl.1999.86.2.441
10.1152/ajpheart.1997.273.6.H2575
10.1152/ajpheart.1991.260.3.H662
10.1152/jappl.1989.66.2.653
10.1152/ajpcell.1995.269.6.C1371
10.1152/ajpheart.1999.276.3.H1058
10.1007/BF02364653
10.1038/227680a0
10.1152/jappl.1996.81.2.686
10.1113/jphysiol.1993.sp019614
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Keywords Regional blood flow
Rat
Enzyme
Arteriole
Rodentia
Environmental factor
Weightlessness
Gene expression
Nitric-oxide synthase
Vasodilation
Endothelium
Microcirculation
Vertebrata
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  doi: 10.1161/01.CIR.99.22.2951
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  doi: 10.1152/ajpheart.2000.278.1.H233
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  doi: 10.1152/jappl.1999.87.4.1476
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  doi: 10.2307/1307797
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  doi: 10.1161/01.RES.22.1.83
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  doi: 10.1152/jappl.1994.76.5.2241
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  doi: 10.1152/jappl.1987.63.2.558
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  doi: 10.1152/jappl.1995.78.6.2079
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  doi: 10.1152/jappl.1995.79.5.1762
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  doi: 10.1152/jappl.1999.86.4.1178
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  doi: 10.1152/jappl.1992.72.6.2210
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  doi: 10.1152/jappl.1997.82.5.1488
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  doi: 10.1016/0076-6879(69)13005-0
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  doi: 10.1152/jappl.1999.86.2.441
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  doi: 10.1152/ajpheart.1997.273.6.H2575
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  start-page: 419
  year: 1985
  ident: B5
  publication-title: Aviat Space Environ Med
  contributor:
    fullname: Dunn CD
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  doi: 10.1152/ajpheart.1991.260.3.H662
– ident: B16
  doi: 10.1152/jappl.1989.66.2.653
– volume: 62
  start-page: 1147
  year: 1991
  ident: B26
  publication-title: Aviat Space Environ Med
  contributor:
    fullname: Woodman CR
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  doi: 10.1152/ajpcell.1995.269.6.C1371
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  doi: 10.1152/ajpheart.1999.276.3.H1058
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  doi: 10.1007/BF02364653
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  doi: 10.1038/227680a0
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  doi: 10.1152/jappl.1996.81.2.686
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  doi: 10.1113/jphysiol.1993.sp019614
– volume: 274
  start-page: H1397
  year: 1998
  ident: B13
  publication-title: Am J Physiol Heart Circ Physiol
  contributor:
    fullname: Moffitt JA
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Snippet Departments of Physiology and Veterinary Biomedical Sciences and Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211 The...
The purpose of this study was to test the hypothesis that endothelium-dependent dilation is impaired in soleus resistance arteries from hindlimb-unweighted...
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StartPage 1483
SubjectTerms Acetylcholine - pharmacology
Animals
Arterioles - drug effects
Arterioles - physiology
Biological and medical sciences
Blood vessels
Blood vessels and receptors
Endothelium, Vascular - drug effects
Endothelium, Vascular - physiology
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Enzymologic - drug effects
Gene Expression Regulation, Enzymologic - physiology
Hindlimb Suspension
In Vitro Techniques
Indomethacin - pharmacology
Male
Muscle, Skeletal - blood supply
Muscular system
Nitric Oxide Synthase - genetics
Nitric Oxide Synthase Type III
Nitroarginine - pharmacology
Nitroprusside - pharmacology
Rats
Rats, Sprague-Dawley
Reference Values
Reverse Transcriptase Polymerase Chain Reaction
Rodents
Space life sciences
Transcription, Genetic - drug effects
Transcription, Genetic - physiology
Vasodilation - drug effects
Vasodilation - physiology
Vertebrates: cardiovascular system
Title Hindlimb unweighting alters endothelium-dependent vasodilation and ecNOS expression in soleus arterioles
URI http://jap.physiology.org/cgi/content/abstract/89/4/1483
https://www.ncbi.nlm.nih.gov/pubmed/11007586
https://www.proquest.com/docview/222145892
https://search.proquest.com/docview/27561032
https://search.proquest.com/docview/72297865
Volume 89
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