Decreased blood pressure in NOX1-deficient mice

被引:259
作者
Gavazzi, G
Banfi, B
Deffert, C
Fiette, L
Schappi, M
Herrmann, F
Krause, KH
机构
[1] Geneva Med Fac, Dept Rehabil & Geriatr, CH-1211 Geneva 4, Switzerland
[2] Geneva Med Fac, Dept Pathol & Immunol, CH-1211 Geneva 4, Switzerland
[3] Geneva Med Fac, Dept Pediat, CH-1211 Geneva 4, Switzerland
[4] Univ Iowa, Coll Med, Dept Anat, Coralville, IA 52241 USA
来源
FEBS LETTERS | 2006年 / 580卷 / 02期
关键词
NOX1; NADPH oxidase; blood pressure; angiotensin II; extraacellular matrix;
D O I
10.1016/j.febslet.2005.12.049
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
To understand the role of the superoxide-generating NADPH oxidase NOX1 in the vascular system, we have generated NOX1-deficient mice. NOX1-deficient mice had a moderately decreased basal blood pressure. In response to angiotensin 11 they showed an almost complete loss of the sustained blood pressure response, while the initial increase was conserved. NOXI-deficient mice showed a marked reduction in aortic media hypertrophy. Angiotensin II-induced smooth muscle cell proliferation was conserved, but there was a marked decrease in extracellular matrix accumulation. Our results establish a role for NOX1 in blood pressure regulation and vascular angiotensin 11 response. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:497 / 504
页数:8
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