A possible role of nitric oxide (NO) in stress-related feeding was investigated in male rats using the tail-pinch (TP) model, in within-subjects experimental designs. An initial experiment demonstrated a dose-related reduction in TP-induced solid food intake over a 10-min test period with increasing dose (10.25, and 50 mg/kg SC) of the NO-synthase (NOS) inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), reaching statistical significance at 25 mg/kg L-NAME when compared to vehicle control (p < 0.05). Pattern analysis further revealed a decrease both in total duration of food-directed oral behavior and in percentage of longer duration (> 60 s) oral behavior bouts with increasing dose of L-NAME; both measures reached statistical significance at 50 mg/kg (p < 0.01). Pretreatment with 500 mg/kg of the NO precursor, L-arginine (L-arg), resulted in partial but not significant reversal of the attenuating effect of 25 mg/kg L-NAME on food intake. Latency to begin eating or gnawing was not significantly affected by L-NAME. In a subsequent experiment, L-arg alone (500 and 750 mg/kg) did not significantly alter TP-induced food intake. It is cautiously suggested that these results implicate involvement of NO in TP-induced feeding.