Short-term increases in pressure and shear stress attenuate age-related declines in endothelial function in skeletal muscle feed arteries

• Published in: European journal of applied physiology Vol. 116; no. 7; pp. 1305 - 1311
• Main Authors: Seawright, John W., Luttrell, Meredith, Trache, Andreea, Woodman, Christopher R.
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.07.2016; Springer Nature B.V
• Subjects: 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; United States > US; Texas; Endothelial dysfunction; Aging; Fischer 344 rats; Vascular smooth muscle; ACh-induced dilation; Skeletal muscle feed arteries
• ISSN: 1439-6319; 1439-6327
• DOI: 10.1007/s00421-016-3388-9

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.