Reactive oxygen species and glucocorticoid-induced hypertension.
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.
Ong
Sharon L H
SL
High Blood Pressure Research Unit, John Curtin School of Medical Research, Australian National University, Canberra, Australian Capital Territory, Australia.
Zhang
Yi
Y
Whitworth
Judith A
JA
D000818:Animals; D005938:Glucocorticoids / Q000494:pharmacology*; D006801:Humans; D006973:Hypertension / Q000139:chemically induced*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism*
D005938:Glucocorticoids; D017382:Reactive Oxygen Species