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REACTIVE OXYGEN SPECIES AND GLUCOCORTICOID‐INDUCED HYPERTENSION
Author(s) -
Ong Sharon LH,
Zhang Yi,
Whitworth Judith A
Publication year - 2008
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2008.04900.x
Subject(s) - xanthine oxidase , oxidative stress , reactive oxygen species , nadph oxidase , enos , nitric oxide , chemistry , superoxide , glucocorticoid , endocrinology , medicine , nitric oxide synthase , biochemistry , biology , enzyme
SUMMARY1 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.