Short-term increases in pressure and shear stress attenuate age-related declines in endothelial function in skeletal muscle feed arteries
Purpose We tested the hypothesis that exposure to a short-term (1 h) increase in intraluminal pressure and shear stress (SS), to mimic two mechanical signals associated with a bout of exercise, improves nitric oxide (NO)-mediated endothelium-dependent dilation in aged soleus muscle feed arteries (SF...
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Published in | European journal of applied physiology Vol. 116; no. 7; pp. 1305 - 1311 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.07.2016
Springer Nature B.V |
Subjects | |
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Abstract | Purpose
We tested the hypothesis that exposure to a short-term (1 h) increase in intraluminal pressure and shear stress (SS), to mimic two mechanical signals associated with a bout of exercise, improves nitric oxide (NO)-mediated endothelium-dependent dilation in aged soleus muscle feed arteries (SFA). In addition, we hypothesized that pressure and SS would interact to produce greater improvements in endothelial function than pressure alone.
Methods
SFA from young (4 months) and old (24 months) Fischer 344 rats were cannulated and pressurized at 90 (P90) or 130 (P130) cmH
2
O and exposed to no SS (0 dyn/cm
2
) or high SS (~65 dyn/cm
2
) for 1 h. At the end of the 1 h treatment period, pressure in all P130 SFA was set to 90 cmH
2
O and no SS (0 dyn/cm
2
) for examination of endothelium-dependent [flow and acetylcholine (ACh)] and endothelium-independent [sodium nitroprusside (SNP)] dilation. To evaluate the contribution of NO, vasodilator responses were assessed in the presence of N
ω
-nitro-
l
-arginine (L-NNA).
Results
Flow- and ACh-induced dilations were impaired in Old P90 SFA. Treatment with increased pressure + SS for 1 h improved flow- and ACh-induced dilations in old SFA. The beneficial effect of pressure + SS was abolished in the presence of L-NNA and was not greater than treatment with increased pressure alone.
Conclusion
These results indicate that short-duration increases in pressure + SS improve NO-mediated endothelium-dependent dilation in aged SFA; however, pressure and SS do not interact to produce greater improvements in endothelial function than pressure alone. |
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AbstractList | We tested the hypothesis that exposure to a short-term (1 h) increase in intraluminal pressure and shear stress (SS), to mimic two mechanical signals associated with a bout of exercise, improves nitric oxide (NO)-mediated endothelium-dependent dilation in aged soleus muscle feed arteries (SFA). In addition, we hypothesized that pressure and SS would interact to produce greater improvements in endothelial function than pressure alone. SFA from young (4 months) and old (24 months) Fischer 344 rats were cannulated and pressurized at 90 (P90) or 130 (P130) cmH sub(2)O and exposed to no SS (0 dyn/cm super(2)) or high SS (~65 dyn/cm super(2)) for 1 h. At the end of the 1 h treatment period, pressure in all P130 SFA was set to 90 cmH sub(2)O and no SS (0 dyn/cm super(2)) for examination of endothelium-dependent [flow and acetylcholine (ACh)] and endothelium-independent [sodium nitroprusside (SNP)] dilation. To evaluate the contribution of NO, vasodilator responses were assessed in the presence of N super( omega )-nitro- sub( l )-arginine (L-NNA). Flow- and ACh-induced dilations were impaired in Old P90 SFA. Treatment with increased pressure + SS for 1 h improved flow- and ACh-induced dilations in old SFA. The beneficial effect of pressure + SS was abolished in the presence of L-NNA and was not greater than treatment with increased pressure alone. These results indicate that short-duration increases in pressure + SS improve NO-mediated endothelium-dependent dilation in aged SFA; however, pressure and SS do not interact to produce greater improvements in endothelial function than pressure alone. We tested the hypothesis that exposure to a short-term (1 h) increase in intraluminal pressure and shear stress (SS), to mimic two mechanical signals associated with a bout of exercise, improves nitric oxide (NO)-mediated endothelium-dependent dilation in aged soleus muscle feed arteries (SFA). In addition, we hypothesized that pressure and SS would interact to produce greater improvements in endothelial function than pressure alone. SFA from young (4 months) and old (24 months) Fischer 344 rats were cannulated and pressurized at 90 (P90) or 130 (P130) cmH2O and exposed to no SS (0 dyn/cm(2)) or high SS (~65 dyn/cm(2)) for 1 h. At the end of the 1 h treatment period, pressure in all P130 SFA was set to 90 cmH2O and no SS (0 dyn/cm(2)) for examination of endothelium-dependent [flow and acetylcholine (ACh)] and endothelium-independent [sodium nitroprusside (SNP)] dilation. To evaluate the contribution of NO, vasodilator responses were assessed in the presence of N(ω)-nitro- l -arginine (L-NNA). Flow- and ACh-induced dilations were impaired in Old P90 SFA. Treatment with increased pressure + SS for 1 h improved flow- and ACh-induced dilations in old SFA. The beneficial effect of pressure + SS was abolished in the presence of L-NNA and was not greater than treatment with increased pressure alone. These results indicate that short-duration increases in pressure + SS improve NO-mediated endothelium-dependent dilation in aged SFA; however, pressure and SS do not interact to produce greater improvements in endothelial function than pressure alone. PURPOSEWe tested the hypothesis that exposure to a short-term (1 h) increase in intraluminal pressure and shear stress (SS), to mimic two mechanical signals associated with a bout of exercise, improves nitric oxide (NO)-mediated endothelium-dependent dilation in aged soleus muscle feed arteries (SFA). In addition, we hypothesized that pressure and SS would interact to produce greater improvements in endothelial function than pressure alone.METHODSSFA from young (4 months) and old (24 months) Fischer 344 rats were cannulated and pressurized at 90 (P90) or 130 (P130) cmH2O and exposed to no SS (0 dyn/cm(2)) or high SS (~65 dyn/cm(2)) for 1 h. At the end of the 1 h treatment period, pressure in all P130 SFA was set to 90 cmH2O and no SS (0 dyn/cm(2)) for examination of endothelium-dependent [flow and acetylcholine (ACh)] and endothelium-independent [sodium nitroprusside (SNP)] dilation. To evaluate the contribution of NO, vasodilator responses were assessed in the presence of N(ω)-nitro- l -arginine (L-NNA).RESULTSFlow- and ACh-induced dilations were impaired in Old P90 SFA. Treatment with increased pressure + SS for 1 h improved flow- and ACh-induced dilations in old SFA. The beneficial effect of pressure + SS was abolished in the presence of L-NNA and was not greater than treatment with increased pressure alone.CONCLUSIONThese results indicate that short-duration increases in pressure + SS improve NO-mediated endothelium-dependent dilation in aged SFA; however, pressure and SS do not interact to produce greater improvements in endothelial function than pressure alone. Purpose We tested the hypothesis that exposure to a short-term (1 h) increase in intraluminal pressure and shear stress (SS), to mimic two mechanical signals associated with a bout of exercise, improves nitric oxide (NO)-mediated endothelium-dependent dilation in aged soleus muscle feed arteries (SFA). In addition, we hypothesized that pressure and SS would interact to produce greater improvements in endothelial function than pressure alone. Methods SFA from young (4 months) and old (24 months) Fischer 344 rats were cannulated and pressurized at 90 (P90) or 130 (P130) cmH2O and exposed to no SS (0 dyn/cm2) or high SS (~65 dyn/cm2) for 1 h. At the end of the 1 h treatment period, pressure in all P130 SFA was set to 90 cmH2O and no SS (0 dyn/cm2) for examination of endothelium-dependent [flow and acetylcholine (ACh)] and endothelium-independent [sodium nitroprusside (SNP)] dilation. To evaluate the contribution of NO, vasodilator responses were assessed in the presence of N[omega]-nitro-l-arginine (L-NNA). Results Flow- and ACh-induced dilations were impaired in Old P90 SFA. Treatment with increased pressure + SS for 1 h improved flow- and ACh-induced dilations in old SFA. The beneficial effect of pressure + SS was abolished in the presence of L-NNA and was not greater than treatment with increased pressure alone. Conclusion These results indicate that short-duration increases in pressure + SS improve NO-mediated endothelium-dependent dilation in aged SFA; however, pressure and SS do not interact to produce greater improvements in endothelial function than pressure alone. Purpose We tested the hypothesis that exposure to a short-term (1 h) increase in intraluminal pressure and shear stress (SS), to mimic two mechanical signals associated with a bout of exercise, improves nitric oxide (NO)-mediated endothelium-dependent dilation in aged soleus muscle feed arteries (SFA). In addition, we hypothesized that pressure and SS would interact to produce greater improvements in endothelial function than pressure alone. Methods SFA from young (4 months) and old (24 months) Fischer 344 rats were cannulated and pressurized at 90 (P90) or 130 (P130) cmH 2 O and exposed to no SS (0 dyn/cm 2 ) or high SS (~65 dyn/cm 2 ) for 1 h. At the end of the 1 h treatment period, pressure in all P130 SFA was set to 90 cmH 2 O and no SS (0 dyn/cm 2 ) for examination of endothelium-dependent [flow and acetylcholine (ACh)] and endothelium-independent [sodium nitroprusside (SNP)] dilation. To evaluate the contribution of NO, vasodilator responses were assessed in the presence of N ω -nitro- l -arginine (L-NNA). Results Flow- and ACh-induced dilations were impaired in Old P90 SFA. Treatment with increased pressure + SS for 1 h improved flow- and ACh-induced dilations in old SFA. The beneficial effect of pressure + SS was abolished in the presence of L-NNA and was not greater than treatment with increased pressure alone. Conclusion These results indicate that short-duration increases in pressure + SS improve NO-mediated endothelium-dependent dilation in aged SFA; however, pressure and SS do not interact to produce greater improvements in endothelial function than pressure alone. |
Author | Luttrell, Meredith Woodman, Christopher R. Trache, Andreea Seawright, John W. |
Author_xml | – sequence: 1 givenname: John W. surname: Seawright fullname: Seawright, John W. organization: Department of Health and Kinesiology, MS 4243, Texas A&M University – sequence: 2 givenname: Meredith surname: Luttrell fullname: Luttrell, Meredith organization: Department of Health and Kinesiology, MS 4243, Texas A&M University – sequence: 3 givenname: Andreea surname: Trache fullname: Trache, Andreea organization: Department of Medical Physiology, Texas A&M University, Department of Biomedical Engineering, Texas A&M University – sequence: 4 givenname: Christopher R. surname: Woodman fullname: Woodman, Christopher R. email: woodmanc@hlkn.tamu.edu organization: Department of Health and Kinesiology, MS 4243, Texas A&M University, Department of Veterinary Physiology and Pharmacology, Texas A&M University |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27146170$$D View this record in MEDLINE/PubMed |
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Keywords | Endothelial dysfunction Aging Fischer 344 rats Vascular smooth muscle ACh-induced dilation Skeletal muscle feed arteries |
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We tested the hypothesis that exposure to a short-term (1 h) increase in intraluminal pressure and shear stress (SS), to mimic two mechanical signals... We tested the hypothesis that exposure to a short-term (1 h) increase in intraluminal pressure and shear stress (SS), to mimic two mechanical signals... Purpose We tested the hypothesis that exposure to a short-term (1 h) increase in intraluminal pressure and shear stress (SS), to mimic two mechanical signals... PURPOSEWe tested the hypothesis that exposure to a short-term (1 h) increase in intraluminal pressure and shear stress (SS), to mimic two mechanical signals... We tested the hypothesis that exposure to a short-term (1 h) increase in intraluminal pressure and shear stress (SS), to mimic two mechanical signals... |
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SubjectTerms | Age Aging Aging - physiology Animals Arterial Pressure - physiology Arteries - physiology Biomedical and Life Sciences Biomedicine Endothelium Endothelium, Vascular - physiology Feeds Female Human Physiology Hypotheses Laboratory animals Male Muscle, Skeletal - blood supply Muscle, Skeletal - physiology Musculoskeletal system Nitric oxide Nitric Oxide - metabolism Occupational Medicine/Industrial Medicine Original Article Physiology Rats Rats, Inbred F344 Shear Strength - physiology Shear stress Sports Medicine Veins & arteries Veterinary medicine |
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Title | Short-term increases in pressure and shear stress attenuate age-related declines in endothelial function in skeletal muscle feed arteries |
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