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Decreased blood pressure in NOX1‐deficient mice
Author(s) -
Gavazzi Gaetan,
Banfi Botond,
Deffert Christine,
Fiette Laurence,
Schappi Michela,
Herrmann Francois,
Krause Karl-Heinz
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.12.049
Subject(s) - nox1 , angiotensin ii , blood pressure , renin–angiotensin system , medicine , endocrinology , muscle hypertrophy , nadph oxidase , vascular remodelling in the embryo , basal (medicine) , chemistry , biology , oxidative stress , insulin
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 II they showed an almost complete loss of the sustained blood pressure response, while the initial increase was conserved. NOX1‐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 II response.