期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 279, 期 5, 页码 H2234-H2240出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.2000.279.5.H2234
关键词
hypertension; superoxide anion; free radicals; reactive oxygen species; NAD(P)H oxidase; NAD(P)H oxidoreductase
资金
- NHLBI NIH HHS [HL-28982, R01 HL-55425] Funding Source: Medline
Although NAD( P)H oxidase-derived superoxide (O-2(-)) is increased during the development of angiotensin II (ANG II)-dependent hypertension, vascular regulation at the protein level has not been reported. We have shown that four major components of NAD( P) H oxidase are located primarily in the vascular adventitia as a primary source of vascular O-2(-). Here we compare vascular levels of O-2(-) and NAD( P) H oxidase in normotensive and ANG II-infused hypertensive mice and show that, after 7 days of ANG II infusion (750 mug.kg(-1).day(-1) ip) in C57B1/6 mice, systolic blood pressure was increased compared with that after sham infusion, concomitant with increased O-2(-) in the thoracic aorta as measured using lucigenin (25 muM)-enhanced chemiluminescence. Both p67(phox) and gp91(phox) were detectable by Western blotting in aortic homogenates, and we observed increased protein levels of NAD( P) H oxidase subunits. These ANG II-induced increases were normalized by simultaneous treatment with the AT(1) receptor antagonist losartan. Moreover, the primary location of these subunits was the adventitia as detected immunohistochemically. Our results suggest that ANG II-induced increases in O-2(-) are due to increased adventitial NAD( P) H oxidase activity, brought about by the heightened expression and interaction of its components.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据