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Role of gp91phox-containing NADPH oxidase in the deoxycorticosterone acetate-salt-induced hypertension.

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.
AuthorsAya Fujii, Daisuke Nakano, Miyuki Katsuragi, Mamoru Ohkita, Masanori Takaoka, Yukihiro Ohno, Yasuo Matsumura
JournalEuropean journal of pharmacology (Eur J Pharmacol) Vol. 552 Issue 1-3 Pg. 131-4 (Dec 15 2006) ISSN: 0014-2999 [Print] Netherlands
PMID17064681 (Publication Type: Journal Article)
Chemical References
  • Membrane Glycoproteins
  • Superoxides
  • Desoxycorticosterone
  • Cybb protein, mouse
  • NADPH Oxidase 2
  • NADPH Oxidases
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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