DMD and Duchenne muscular dystrophy: Despite these limitations, our findings indicate that simply delivering exogenous NO via HCT 1026 to mdx mice, which like DMD patients lack all components of the dystrophin-glycoprotein complex, fully replicates the physiological role of sarcolemmal nNOSμ-derived NO to modulate α-adrenergic vasoconstriction in exercising muscle.