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• W2007045655 abstract "Coronary vasodilation is impaired in the postischemic heart with a loss of endothelial nitric oxide synthase (eNOS) activity, but the mechanisms underlying ischemia-induced eNOS dysfunction are not understood. For nitric oxide (NO) synthesis, eNOS requires the redox-sensitive cofactor tetrahydrobiopterin (BH 4 ); however, the role of BH 4 in ischemia-induced endothelial dysfunction remains unknown. Therefore, isolated rat hearts were subjected to varying durations of ischemia, and the alterations in NOS-dependent vasodilation were measured and correlated with assays of eNOS activity and cardiac BH 4 concentrations. Ischemia time-dependently decreased cardiac BH 4 content with 85, 95, or 97% irreversible degradation after 30, 45, or 60 min of ischemia, respectively. Paralleling the decreases in BH 4 , reductions of eNOS activity were seen of 58, 86, or 92%, and NOS-derived superoxide production was greatly increased. Addition of 10 μM BH 4 enhanced eNOS activity in nonischemic hearts and partially restored activity after ischemia. It also suppressed NOS-derived superoxide production. Impaired coronary flow during postischemic reperfusion was improved by BH 4 infusion. Thus, BH 4 depletion contributes to postischemic eNOS dysfunction, and BH 4 treatment is effective in partial restoration of endothelium-dependent coronary flow. Supplementation of BH 4 may therefore be an important therapeutic approach to reverse endothelial dysfunction in postischemic tissues." @default.
• W2007045655 created "2016-06-24" @default.
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• W2007045655 date "2007-09-18" @default.
• W2007045655 modified "2023-10-16" @default.
• W2007045655 title "Myocardial ischemia results in tetrahydrobiopterin (BH ₄ ) oxidation with impaired endothelial function ameliorated by BH ₄" @default.
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• W2007045655 doi "https://doi.org/10.1073/pnas.0702986104" @default.
• W2007045655 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1986616" @default.
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• W2007045655 hasPublicationYear "2007" @default.
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