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

• Published in: Pharmacology, biochemistry and behavior Vol. 60; no. 3; pp. 601 - 607
• Main Author: CZECH, D. A
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Science 01-07-1998
• Subjects: Animals; Behavioral psychophysiology; Biological and medical sciences; Dose-Response Relationship, Drug; Drinking - drug effects; Enzyme Inhibitors - pharmacology; Feeding Behavior - drug effects; Fundamental and applied biological sciences. Psychology; Glucose - deficiency; Hypoglycemic Agents - pharmacology; Insulin - pharmacology; Male; Mice; Mice, Inbred ICR; Neurotransmission and behavior; Nitric Oxide Synthase - antagonists & inhibitors; Nitroarginine - pharmacology; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Water Deprivation - physiology; Feeding behavior; Enzyme; Rodentia; Enzyme inhibitor; Drinking; Nitric-oxide synthase; Vertebrata; Mammalia; Neuromodulator; Mouse; Food intake; Animal; Nitric oxide; Oxidoreductases; Hyperphagia
• EISSN: 1873-5177
• ISSN: 0091-3057

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.