Nitric oxide release is present from incubated skeletal muscle preparations.

To determine whether nitric oxide (NO) synthase activity exists in rat skeletal muscle, media from incubated rat extensor digitorum longus muscle preparations were assayed for NO with a chemiluminescent detection system. Although small amounts of NO were detected in media alone, the addition of muscle increased NO concentration in the media by 30-fold. The release of NO into the media diminished over time. Either arginine (10(-6) M), sodium nitroprusside (10(-6) M), or prior electrical stimulation in vivo caused 50-200% increases (P < 0.05) in NO concentration. NG-monomethyl-L-arginine monoacetate (10(-6) M), an NO synthase inhibitor, decreased both basal 2-deoxyglucose transport and NO efflux, indicating that NO may play a role in modulating skeletal muscle carbohydrate metabolism. These data indicate that NO is released from an incubated skeletal muscle preparation and presents the possibility that muscle-derived NO may play an important metabolic role.