OR-46: Angiotensin II (Ang II) stimulates sympathetic nerve (SNS) activity through activation of oxidative stress

• Published in: American journal of hypertension 2003-05, Vol.16 (S1), p.21A-21A
• Main Authors: Campese, Vito M., Ye, Shaohua, Zhong, Huiquin
• Format: Article
• Language: English
• Subjects: Angiotensin II; Oxidative stress; Sympathetic nervous system
• ISSN: 0895-7061; 1941-7225
• DOI: 10.1016/S0895-7061(03)00130-4

There is substantial evidence that Ang II enhances SNS activity. The mechanisms of central SNS activation are not well established. We have shown that infusion of Ang II in the lateral ventricle (ICV) raises blood pressure (BP), renal SNS activity (RSNA), and norepinephrine (NE) secretion from the posterior hypothalamic nuclei (PH). Ang II also reduces the abundance of interleukin (IL-1β) and nNOS mRNA in the PH. Pretreatment with losartan, a (AT1) receptor antagonist, abolishes these effects of Ang II. These studies suggest that Ang II-induced decrease in NO expression may be responsible for SNS activation. In the current studies we have tested the hypothesis that the effects of Ang II on NO and SNS activity are mediated by increased oxidative stress. To test this hypothesis, we infused tempol, a superoxide dismutase mimetic, (50 mg/ Kg body weight/min, ICV) prior to Ang II (at the rate of 1.67 mg/mL/Kg/min x 60 min). Ang II raised BP from 110±1.0 to 127±1.2 mmHg (P