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  • Title: Hydrogen peroxide potentiates the EDHF phenomenon by promoting endothelial Ca2+ mobilization.
    Author: Edwards DH, Li Y, Griffith TM.
    Journal: Arterioscler Thromb Vasc Biol; 2008 Oct; 28(10):1774-81. PubMed ID: 18669883.
    Abstract:
    OBJECTIVE: The purpose of this study was to test the hypothesis that H(2)O(2) contributes to the EDHF phenomenon by mobilizing endothelial Ca(2+) stores. METHODS AND RESULTS: Myograph studies with rabbit iliac arteries demonstrated that EDHF-type relaxations evoked by the SERCA inhibitor cyclopiazonic acid (CPA) required activation of K(Ca) channels and were potentiated by exogenous H(2)O(2) and the thiol oxidant thimerosal. Preincubation with a submaximal concentration of CPA unmasked an ability of exogenous H(2)O(2) to stimulate an EDHF-type response that was sensitive to K(Ca) channel blockade. Imaging of cytosolic and endoplasmic reticulum [Ca(2+)] in rabbit aortic valve endothelial cells with Fura-2 and Mag-fluo-4 demonstrated that H(2)O(2) and thimerosal, which sensitizes the InsP(3) receptor, both enhanced CPA-evoked Ca(2+) release from stores, and that the potentiating effect of H(2)O(2) was suppressed by the cell-permeant thiol reductant glutathione monoethylester. CPA-evoked relaxations were attenuated by exogenous catalase and potentiated by the catalase inhibitor 3-aminotriazole, and were abolished by the connexin-mimetic peptide (43)Gap26, which interrupts intercellular communication via gap junctions constructed from connexin 43. CONCLUSIONS: H(2)O(2) can enhance EDHF-type relaxations by potentiating Ca(2+) release from endothelial stores, probably via redox modification of the InsP(3) receptor, leading to the opening of hyperpolarizing endothelial K(Ca) channels and an electrotonically-mediated relaxant response.
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