Analysis of agonist-evoked nitric oxide release from human endothelial cells: role of superoxide anion

Clinical and Experimental Pharmacology & Physiology
M David-DufilhoM A Devynck

Abstract

1. Dichlorofluorescein oxidation and electrochemical monitoring of in situ nitric oxide (NO) release from cultured human endothelial cells reveals that agonists such as thrombin and histamine simultaneously stimulate transient superoxide production. 2. The duration of *NO release was increased only in the simultaneous presence of extracellular L-arginine and exogenous superoxide dismutase. In contrast, the inhibition of membrane reduced nicotinamide adenine dinucleotide (phosphate) oxidases, the major source of *O2- in endothelial cells, did not prolong *NO release, although extracellular L-arginine was also present. Comparison of these two experimental conditions suggested that H2O2 was involved in the extension of the *NO signal. 3. The present study demonstrates that, in the absence of external L-arginine, *O2- production does not constitute the major pathway controlling the duration of agonist-induced *NO signal. These results suggest that L-arginine and H2O2 act jointly to maintain nitric oxide synthase in an activated form.

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Citations

Feb 8, 2003·Endothelium : Journal of Endothelial Cell Research·James R Stone, Tucker Collins
Jun 9, 2004·Free Radical Biology & Medicine·Gökce TopalMonique David-Dufilho
Jun 28, 2006·The Journal of Pharmacology and Experimental Therapeutics·Gökce TopalMonique David-Dufilho
Dec 30, 2004·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Mamadou NdiayeValérie B Schini-Kerth

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