Reactive oxygen species and glucocorticoid-induced hypertension

Sharon L.H. Ong, Yi Zhang, Judith A. Whitworth*

*Corresponding author for this work

    Research output: Contribution to journalArticlepeer-review

    35 Citations (Scopus)

    Abstract

    1. There is increasing evidence for a role of oxidative stress and nitric oxide deficiency in experimental glucocorticoid-induced hypertension, as evidenced by increased biomarkers of oxidative stress; the effectiveness of antioxidants or reduced NADPH oxidase antagonists in lowering blood pressure; and secondary upregulation of endogenous antioxidant enzymes in response to oxidative stress. 2. In the vasculature, the main sources of superoxide are NADPH oxidase, xanthine oxidase, uncoupled endothelial nitric oxide synthase (eNOS) and mitochondria. 3. NADPH oxidase plays a significant role in the pathogenesis of glucocorticoid-induced hypertension in the rats, but xanthine oxidase and uncoupled eNOS pathways are not important sources of reactive oxygen species in these models. The role of mitochondrial reactive oxygen species in glucocorticoid-induced hypertension remains to be clarified.

    Original languageEnglish
    Pages (from-to)477-482
    Number of pages6
    JournalClinical and Experimental Pharmacology and Physiology
    Volume35
    Issue number4
    DOIs
    Publication statusPublished - Apr 2008

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