Mechanisms and consequences of endothelial nitric oxide synthase dysfunction in hypertension

J Hypertens. 2015 Jun;33(6):1128-36. doi: 10.1097/HJH.0000000000000587.

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Antihypertensive Agents / therapeutic use
  • Biopterin / analogs & derivatives
  • Biopterin / metabolism
  • Blood Pressure / physiology
  • Endothelium, Vascular / physiopathology*
  • Humans
  • Hypertension / drug therapy
  • Hypertension / enzymology*
  • Nitric Oxide / biosynthesis
  • Nitric Oxide Synthase Type III / drug effects
  • Nitric Oxide Synthase Type III / metabolism*
  • Oxidative Stress / drug effects
  • Reactive Oxygen Species / metabolism
  • Superoxides / metabolism

Substances

  • Antihypertensive Agents
  • Reactive Oxygen Species
  • Superoxides
  • Biopterin
  • Nitric Oxide
  • Nitric Oxide Synthase Type III
  • sapropterin