Possible involvement of nitric oxide (NO) in glucoprivic hyperphagia was investigated in nondeprived male ICR mice in independent groups designs. One pair of experiments demonstrated dose-related reductions in 2-deoxy-D-glucose (2DG)- and insulin-induced solid food intake with increasing dose (10, 25, and 50 mg/kg s.c.) of the NO-synthase (NOS) inhibitor, NG-nitro-L-arginine (L-NOARG), reaching statistical significance at 10 mg/kg L-NOARG when compared to vehicle controls. In a second pair of experiments, initial pretreatment with L-arginine (500 and 1000 mg/kg i.p.) partially or completely restored the feeding inhibitory action of an effective challenge dose (25 mg/kg) of L-NOARG; D-arginine (500 mg/kg i.p.) was ineffective, thus supporting a stereospecific action of arginine. A third set of experiments demonstrated dose-related reduction in glucoprivic feeding under delayed access (4 or 6 h) to food. These findings suggest involvement of NO in glucoprivic hyperphagia; they are consistent with and extend research linking NO and ingestive behaviors through use of NOS inhibitors. Deprivation-induced drinking was attenuated by these doses of L-NOARG as well.