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1 Department of Pathophysiology, Semmelweis University, Budapest, Hungary
2 Department of Pathophysiology, Semmelweis University, Budapest, Hungary; Department of Physiology, New York Medical College, Valhalla, NY, USA
* To whom correspondence should be addressed. E-mail: koller{at}nymc.edu.
We hypothesized that hydrogen peroxide (H2O2) has a role in the local regulation of skeletal muscle blood flow, thus it should have significant effect on the myogenic tone of arterioles. Thus, effects of exogenous H2O2 on the diameter of isolated, pressurized (at 80 mmHg) rat gracilis skeletal muscle arterioles (diameter: ~150 µm) were investigated. Lower concentrations of H2O2 (10-6-3x10-5 M) elicited constrictions, whereas higher concentrations of H2O2 (6x10-5-3x10-4 M), after initial constrictions, caused dilations of arterioles (10-4 M H2O2: -19±1% and 66±4%). Endothelium removal reduced both constrictions (max: -10±1%) and dilations (33±3%) to H2O2. Constrictions to H2O2 were completely abolished by indomethacin and the prostaglandin H2/thromboxane A2 (PGH2/TxA2) receptor antagonist SQ29548. Dilations to H2O2 were significantly reduced by inhibition of NO synthase (to 38±7%) but were unaffected by clotrimazole or sulfaphenazole (inhibitors of CYP450 enzymes), indomethacin or SQ29548. In endothelium-denuded arterioles clotrimazole had no effect, whereas H2O2-induced dilations were significantly reduced by charybdotoxin plus apamin, inhibitors of KCa-channels (to 24±3%) and by glibenclamide selective blocker of KATP channels (to 14±2%), and the non-selective K+-channel inhibitor tetrabutyl-ammonium (to -1±1%). Thus exogenous administration of H2O2 elicits release of 1) PGH2/TxA2 both from endothelium and smooth muscle, 2) NO from the endothelium and 3) activates potassium channels, such as KCa- KATP channels in the smooth muscle resulting in biphasic changes of arteriolar diameter. Because H2O2 already at low micromolar concentrations activates several intrinsic mechanisms we suggest that H2O2 contributes to the local regulation of skeletal muscle blood flow in various physiological and pathophysiological conditions.
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