A NITRIC-OXIDE SYNTHASE INHIBITOR N-G-NITRO-L-ARGININE, ATTENUATES GLUCOPRIVIC FEEDING AND DEPRIVATION-INDUCED DRINKING IN THE MOUSE

Possible involvement of nitric oxide (NO) in glucoprivic hyperphagia w as investigated in nondeprived male ICR mice in independent groups des igns. One pair of experiments demonstrated dose-related reductions in 2-deoxy-D-glucose (2DG)- and insulin-induced solid food intake with in creasing dose (10, 25, and 50 mg/kg SC) of the NO-synthase (NOS) inhib itor, N-G-nitro-L-arginine (L-NOARG), reaching statistical significanc e at 10 mg/kg L-NOARG when compared to vehicle controls. In a second p air of experiments, initial pre treatment with L-arginine (500 and 100 0 mg/kg TP) partially or completely restored the feeding inhibitory ac tion of an effective challenge dose (25 mg/kg) of L-NOARG; D-arginine (500 mg/kg LP) was ineffective, thus supporting a stereospecific actio n of arginine. A third set of experiments demonstrated dose-related re duction 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. (C) 1998 Elsevier S cience Inc.