Acute increases in intraluminal pressure improve vasodilator responses in aged soleus muscle feed arteries

We tested the hypothesis that exposure to an acute increase in intraluminal pressure, to mimic pressure associated with a bout of exercise, improves nitric oxide (NO)-mediated endothelium-dependent dilation in aged soleus muscle feed arteries (SFA) and that improved endothelial function would persist after a 2 h recovery period. SFA from young (4-month) and old (24-month) Fischer 344 rats were cannulated and pressurized at 90 (P90) or 130 (P130) cmH(2)O for 60 min. At the end of the treatment period, pressure in the P130 SFA was lowered to 90 cmH(2)O for examination of endothelium-dependent [flow or acetylcholine (ACh)] and endothelium-independent [sodium nitroprusside (SNP)] vasodilation. To determine the role of NO, vasodilator responses were assessed in the presence of N (omega)-nitro-l-arginine (L-NNA). To determine whether the effects of pressure persisted following a recovery period at normal pressure, SFA were pressurized to 130 cmH(2)O for 60 min and subsequently lowered to 90 cmH(2)O for 2 h before assessing function. ACh- and flow-induced dilations were impaired in old SFA. Treatment with increased pressure for 60 min improved ACh- and flow-induced dilations in old SFA. SNP-induced dilation was improved in old and young SFA. The beneficial effect of pressure treatment on ACh- and flow-induced dilation in old SFA was blocked by L-NNA and was not present following a 2 h recovery period. These results indicate that an acute increase in intraluminal pressure improves NO-mediated endothelium-dependent dilation in aged SFA; however, the beneficial effect does not persist after 2 h.