Diminished bioavailability of nitric oxide (NO) may impair skeletal muscle arteriolar function after myocardial infarction (MI). We tested the hypotheses that chronic MI induced would diminish 1) endothelial function in large (resting diameter ~75μm) feed arterioles, and 2) functional dilation in feed arterioles, but not smaller arcade (~25μm) or transverse (~15μm) arterioles, in the spinotrapezius muscle of female Sprague-Dawley rats. Additionally, we hypothesized that blockade of NO production with NG-nitro-l-arginine methyl ester (l-NAME; 30mg/kg i.v.) would have a greater blunting effect on control rats than MI rats. Endothelial function of the feed arterioles was assessed with an infusion of acetylcholine (1.5μg i.v.) after pretreatment with indomethacin (5mg/kgi.p.). MI blunted the response to acetylcholine in feed arterioles (p=0.037), but did not affect resting or post-contraction diameter at any branching order. l-NAME had similar effects on MI and SHAM rats; the response to acetylcholine was blunted in feed arterioles (p=0.003), resting diameter was diminished in arcade arterioles (p=0.003), and post-contraction diameter was diminished in both arcade arterioles (p=0.03) and transverse arterioles (p=0.05). In conclusion, despite endothelial dysfunction in feed arterioles, functional dilation was not affected by MI in any branching order studied. l-NAME had similar effects on MI and SHAM rats that were branch order-dependent. These branch-order effects should be considered in future studies of the control of blood flow. © 2010 Elsevier Inc.