Mechanisms and consequences of endothelial nitric oxide synthase dysfunction in hypertension.

Abstract:

: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.

journal_name

J Hypertens

journal_title

Journal of hypertension

authors

Li Q,Youn JY,Cai H

doi

10.1097/HJH.0000000000000587

subject

Has Abstract

pub_date

2015-06-01 00:00:00

pages

1128-36

issue

6

eissn

0263-6352

issn

1473-5598

journal_volume

33

pub_type

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