Journal
JOURNAL OF HYPERTENSION
Volume 33, Issue 6, Pages 1128-1136Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/HJH.0000000000000587
Keywords
endothelial dysfunction; endothelial nitric oxide synthase; endothelial nitric oxide synthase uncoupling; hypertension; nicotinamide adenine dinucleotide phosphate oxidase; nitric oxide; oxidative stress; tetrahydrobiopterin
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Funding
- National Institute of Health National Heart, Lung and Blood Institute (NHLBI) [HL077440, HL088975, HL108701, HL119968]
- American Heart Association Established Investigator Award (EIA) [12EIA8990025]
- AHA Postdoctoral Fellowship Award [14POST20380966]
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Reduced nitric oxide bioavailability contributes to endothelial dysfunction and hypertension. The endothelial isoform of nitric oxide synthase (eNOS) is responsible for the production of nitric oxide within the endothelium. Loss of eNOS cofactor tetrahydrobiopterin to initial increase in oxidative stress leads to uncoupling of eNOS, in which the enzyme produces superoxide anion rather than nitric oxide, further substantiating oxidative stress to induce vascular pathogenesis. The current review focuses on recent advances on the molecular mechanisms and consequences of eNOS dysfunction in hypertension, and potential novel therapeutic strategies restoring eNOS function to treat hypertension.
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