Table 2.

Effects of nitric oxide synthase inhibitors on stimulation of hexose uptake by sodium azide and AICAR in Clone 9 cells

2-deoxy-D-glucose uptake (% of basal in absence of inhibitor)3-O-methylglucose uptake (% of basal in absence of inhibitor)
TreatmentBasal5 mM azideBasal500 μM AICAR
No inhibitora 100.0±6.5 470.7±24.0 100.0±41.9 285.5±41.5 
400 μM L-NMMAa 68.3±3.6 324.6±5.6* 41.1±11.6 209.3±23.7 
No inhibitorb 100.0±26.2 761.4±13.8 100.0±51.1 438.9±133.8 
2 mM L-NAMEb 77.4±6.1 554.7±7.1* 138.9±55.7 379.5±23.0 
2-deoxy-D-glucose uptake (% of basal in absence of inhibitor)3-O-methylglucose uptake (% of basal in absence of inhibitor)
TreatmentBasal5 mM azideBasal500 μM AICAR
No inhibitora 100.0±6.5 470.7±24.0 100.0±41.9 285.5±41.5 
400 μM L-NMMAa 68.3±3.6 324.6±5.6* 41.1±11.6 209.3±23.7 
No inhibitorb 100.0±26.2 761.4±13.8 100.0±51.1 438.9±133.8 
2 mM L-NAMEb 77.4±6.1 554.7±7.1* 138.9±55.7 379.5±23.0 

Clone 9 cells were treated with or without 400 μM L-NMMA or 2 mM L-NAME for 60 minutes. During the last 30 minutes of this period they were exposed either to 5 mM sodium azide or 500 μM AICAR or exposed to neither agent(basal). The uptake of [3H]3-O-methyl-D-glucose or[3H]2-deoxy-D-glucose was then measured as described in the Materials and Methods. a,bSeparate batches of cells, which exhibited slightly differing fold-stimulations of transport by azide and AICAR, were used for experiments with L-NMMA and L-NAME. The results shown are the means±s.e.m for three experiments; *this value is significantly different (P<0.05) from azide-stimulated uptake rate in the absence of the inhibitor.

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