Decreased blood pressure in NOX1-deficient mice

被引：253

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

页码：497 / 504

页数：8

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