We tested the hypothesis that short-term increases in intraluminal pressure improve endothelium-dependent dilation and increase endothelial nitric oxide synthase (eNOS) expression in senescent soleus muscle feed arteries (SFA). SFA isolated from young (4 mo) and old (24 mo) Fischer 344 rats were cannulated and pressurized at 90 (p90) or 130 (p130) cm H₂O for 4 h. At the end of the 4-h protocol, pressure in p130 SFA was lowered to 90 cm H₂O for examination of endothelium-dependent [flow or acetylcholine (ACh)] vasodilation. Flow- and ACh-induced dilations were blunted in old p90 SFA relative to young p90 SFA. Pre-treatment with increased pressure (p130) improved flow- and ACh-induced dilations in old SFA such that vasodilator responses were similar to young SFA. In the presence of N-nitro-L-arginine (L-NNA), or L-NNA + indomethacin (Indo), flow-induced dilation was inhibited in old p130 SFA such that the response was not greater than old p90 SFA. In old p130 SFA, ACh-induced dilation was inhibited by L-NNA + Indo (not L-NNA alone). In a separate experiment, SFA were pressurized at 70 (p70), 90 (p90), 110 (p110) or 130 (p130) cm H₂O for 4 h and eNOS mRNA and protein content were assessed. Increased pressure induced eNOS mRNA expression in young (not old) SFA. eNOS protein content was not altered in young or old SFA. These results indicate that short-term increases in intraluminal pressure improve endothelium-dependent dilation in senescent SFA in part by enhancing nitric oxide bioavailability; however, the beneficial effect was not associated with increased eNOS expression.