Short-term increases in pressure and shear stress attenuate age-related declines in endothelial function in skeletal muscle feed arteries.
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PURPOSE: We tested the hypothesis that exposure to a short-term (1h) 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 1h. At the end of the 1h 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()-nitro- l -arginine (L-NNA). RESULTS: Flow- and ACh-induced dilations were impaired in Old P90 SFA. Treatment with increased pressure+SS for 1h 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.
