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1 Department of Physiology, New York Medical College, Valhalla, NY, USA; Department of Pathophysiology, Semmelweis University, Budapest, Hungary
2 Department of Pathophysiology, Semmelweis University, Budapest, Hungary
3 Department of Physiology, New York Medical College, Valhalla, NY, USA
* To whom correspondence should be addressed. E-mail: gabor_kaley{at}nymc.edu.
We hypothesized that transient high glucose concentration (tHG) interferes with mediation by NO of flow-induced dilation (FID) of arterioles due to enhanced production of superoxide. In isolated, pressurized (80 mmHg) rat gracilis muscle arterioles (~150 µm) after tHG (incubation with 30 mmol/L glucose for 1 hour), FID became reduced (max: control: 38±4%; after tHG: 17±3%), which was not further diminished by the NO synthase inhibitor, L-NAME (18±2%). Correspondingly, an enhanced superoxide dismutase (PEG-SOD)-sensitive superoxide production was detected after tHG in carotid arteries by dihydroethydine staining. Presence of PEG-SOD during tHG prevented the reduction of FID (41±3%), which could be inhibited by L-NAME (20±4%). Administration of PEG-SOD after tHG did not prevent the reduction of FID (22±3%). Sepiapterin (a precursor of the NO synthase cofactor BH4), administered during tHG did not prevent the reduction of FID (max: 15±5%), however it restored FID if administered after tHG (32±4%). Furthermore, inhibition of either glycolysis by 2-deoxyglucose or mitochondrial complex II by thenoyl-trifluoroacetone reduced the tHG-induced, DHE-detectable enhanced superoxide production in carotid arteries and prevented the reduction in FID of arterioles (35±2%). Collectively, these findings suggest that in skeletal muscle arterioles a transient elevation of glucose - via its increased metabolism - elicits enhanced production of superoxide, which decreases the bioavailability of NO and the level of the NOS cofactor tetrahydrobiopterin, resulting in a reduction of flow-induced dilation mediated by NO.
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