A nitric oxide synthase inhibitor NG-nitro-L-arginine, attenuates glucoprivic feeding and deprivation-induced drinking in the mouse.

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.