Inhibition of CO(2) production from glucose by arginine in brain slices of rats.

In the present study we evaluated the in vivo effect of arginine on CO(2) production from glucose in a medium with physiological and high extracellular K(+) concentrations. We also tested the influence of the nitric oxide synthase inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), on the effects elicited by arginine in order to investigate the possible participation of NO and/or its derivatives on the effects of arginine on CO(2) production from glucose. Sixty-day-old rats were treated with a single intraperitoneal injection of saline (control; group I), arginine (0.8 g/kg; group II), L-NAME (2.0 mg/kg; group III) or arginine (0.8 g/kg) plus L-NAME (2.0 mg/kg; group IV) and were killed 1 h later. Results showed that arginine administration inhibited CO(2) production from glucose at physiological extracellular K(+) concentration and L-NAME prevented such effect. In contrast, arginine administration had no effect on CO(2) production from glucose at high extracellular K(+) concentration. Based on these data, we also investigated the in vitro effect of arginine on CO(2) production from glucose in a medium with physiological extracellular K(+) concentration in hippocampus slices. Results showed that arginine (0.1-1.5 mM) when added to the incubation medium did not alter CO(2) production from glucose in hippocampus slices of untreated rats. In addition, we also demonstrated that arginine inhibits Na(+), K(+)-ATPase activity. The data indicate that the reduction of CO(2) production by arginine was probably mediated by NO and/or its derivatives, which could act inhibiting the activity of Na(+), K(+)-ATPase. The results suggest that arginine impairs energy metabolism in hippocampus slices of rats.