摘要

Excessive production of reactive oxygen species (ROS) leads to inactivation of nitric oxide (NO) and subsequent endothelial dysfunction. All cardiovascular risk factors (hypertension, dyslipidemia, diabetes, etc.) have been reported to elicit vascular oxidative stress. Angiotensin II (Ang II) is one of the most important mediators of vascular dysfunction in the presence of oxidative stress. Most of the actions of Ang Hun endothelial cells are known to be associated with increased production of superoxide anion (O-2(-)) which is the major responsible for endothelial NO synthase uncoupling. The aim of the present study was to assess the contribution of hydrogen peroxide (H2O2) production in murine vessels to endothelial dysfunction after Aug II treatment. Rat aortic segments were incubated in the presence vs. absence of Ang II or H2O2. Subsequently, the tissue was either studied in organ bath system for the vasomotor function or used for measurements of H2O2 production by the FOX (Ferric iron Xylenol Orange) assay. The results showed an attenuation of vascular relaxation response after Ang II application; this effect was at least partially mediated via the the increased H2O2 generation and involved the impairment of NO production.

  • 出版日期2014-6