Abstract |
NADPH oxidase plays an important role in vascular oxidative stress in hypertensive diseases. We evaluated whether NADPH oxidase-dependent superoxide (O(2)(-)) production is involved in the deoxycorticosterone acetate ( DOCA)- salt-induced hypertension, using mice which are genetically deficient in gp91phox, an NADPH oxidase subunit protein (gp91(-/-) mice). Two weeks after the DOCA- salt treatment, systolic blood pressure was significantly elevated in wild-type mice, but not in gp91(-/-) mice. After a 5-week treatment period, wild-type mice developed high blood pressure, with a systolic blood pressure of 127 +/- 3 mm Hg, compared with 107 +/- 4 mm Hg in gp91(-/-) mice. Aortic O(2)(-) production in wild-type DOCA- salt-treated mice was significantly higher than that in wild-type sham mice, whereas there were no significant differences in aortic O(2)(-) production between gp91(-/-) DOCA- salt-treated and sham mice. These findings suggest that vascular O(2)(-) overproduction via gp91phox-containing NADPH oxidase is one of the crucial factors in the development of DOCA- salt-induced hypertension.
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Authors | Aya Fujii, Daisuke Nakano, Miyuki Katsuragi, Mamoru Ohkita, Masanori Takaoka, Yukihiro Ohno, Yasuo Matsumura |
Journal | European journal of pharmacology
(Eur J Pharmacol)
Vol. 552
Issue 1-3
Pg. 131-4
(Dec 15 2006)
ISSN: 0014-2999 [Print] Netherlands |
PMID | 17064681
(Publication Type: Journal Article)
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Chemical References |
- Membrane Glycoproteins
- Superoxides
- Desoxycorticosterone
- Cybb protein, mouse
- NADPH Oxidase 2
- NADPH Oxidases
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Topics |
- Animals
- Aorta
(drug effects, metabolism)
- Blood Pressure
(drug effects)
- Desoxycorticosterone
(administration & dosage, toxicity)
- Genotype
- Hypertension
(chemically induced, genetics, physiopathology)
- Male
- Membrane Glycoproteins
(deficiency, genetics, physiology)
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- NADPH Oxidase 2
- NADPH Oxidases
(deficiency, genetics, physiology)
- Superoxides
(metabolism)
- Time Factors
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