title: Short-term increases in pressure and shear stress attenuate age-related declines in endothelial function in skeletal muscle feed arteries.
abstract: OBJECTIVE
  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/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).
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Health and Kinesiology, MS 4243, Texas A&M University, College Station, TX, 77843-4243, USA.
authors.forename: John W
authors.initials: JW
authors.lastname: Seawright
authors.affiliation: Department of Health and Kinesiology, MS 4243, Texas A&M University, College Station, TX, 77843-4243, USA.
authors.forename: Meredith
authors.initials: M
authors.lastname: Luttrell
authors.affiliation: Department of Medical Physiology, Texas A&M University, College Station, TX, USA.|Department of Biomedical Engineering, Texas A&M University, College Station, TX, USA.
authors.forename: Andreea
authors.initials: A
authors.lastname: Trache
authors.affiliation: Department of Health and Kinesiology, MS 4243, Texas A&M University, College Station, TX, 77843-4243, USA. woodmanc@hlkn.tamu.edu.|Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, TX, USA. woodmanc@hlkn.tamu.edu.
authors.forename: Christopher R
authors.initials: CR
authors.lastname: Woodman
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D062186:Arterial Pressure / Q000502:physiology*; D001158:Arteries / Q000502:physiology*; D004730:Endothelium, Vascular / Q000502:physiology*; D005260:Female; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism*; D051381:Rats; D011916:Rats, Inbred F344; D033081:Shear Strength / Q000502:physiology
chemical_list: D009569:Nitric Oxide
keywords: ACh-induced dilation; Aging; Endothelial dysfunction; Fischer 344 rats; Skeletal muscle feed arteries; Vascular smooth muscle