We demonstrated an increase of nitric oxide (NO) production in aortas of zucker obese fatty rat (ZOF). Metabolic syndrome is associated with an attenuation of acetylcholine (ACh) response. The impairment of ACh induced vasodilation suggests a decrease in nitric oxide (NO) bioavailability. The aim of this work was to assess whether a reduced NO production is involved in the drop of NO bioavailability. Male zucker obese fatty (ZOF, n=8) and lean (n=9) rats, 31 weeks old, were anesthetized and thoracic aortic segments harvested. The NO produced by aortic rings was assayed by EPR spectroscopy using colloid Fe(DETC)2 spin-trapping. The EPR spectra were obtained using a X-Band EPR spectrometer. Basal NO production was significantly (p=0.0001) increase (126 %) in ZOF rats (3061±201AU/h/mg) from lean controls (1356±101AU/h/mg). Addition of ACh (3.10-6M) induced an increase in NO levels in aortic rings of both ZOF and lean rats, this relative increase was significantly smaller in ZOF (162±10 vs 270±26 %, p=0.002). However the level was higher in ZOF (4905±360 vs 3500±213AU/h/mg, p=0.004). Without endothelium no NO production was detecded in ZOF aortas. A specific inhibitor of neuronal NOS, Nw-Propyl-L-arginine (PLA; 0,1μm), was unable to decreased both NO productions: the basal NO production and the ACh-stimulated NO production in ZOF aortas. A similar result was obtained with the specific inhibitor of inducible NOS suggesting the only involvement of eNOS in increase of NO production observed in ZOF. We conclude that the vascular dysfunction observed in metabolic syndrome is not due to a decrease in NO production but may be at least in part due to a reduced sensitivity to ACh stimulation.Le texte complet de cet article est disponible en PDF.