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gp91^phox-containing NAD(P)H oxidase mediates attenuation of nitric oxide-dependent control of myocardial oxygen consumption by ANG II

Department of Physiology, New York Medical College, Valhalla, New York 10595

Submitted 25 January 2005 ; accepted in final form 11 March 2005

We have previously reported that ANG II stimulation increased superoxide anion (O₂^–) through the activation of NAD(P)H oxidase and inhibited nitric oxide (NO)-dependent control of myocardial oxygen consumption (MO₂) by scavenging NO. Our objective was to investigate the role of NAD(P)H oxidase, especially the gp91^phox subunit, in the NO-dependent control of MO₂. MO₂ in mice with defects in the expression of gp91^phox [gp91^phox(–/–)] was measured with a Clark-type oxygen electrode. Baseline MO₂ was not significantly different between wild-type (WT) and gp91^phox(–/–) mice. Stimulation of NO production by bradykinin (BK) induced significant decreases in MO₂ in WT mice. BK-induced reduction in MO₂ was enhanced in gp91^phox(–/–) mice. BK-induced reduction in MO₂ in WT mice was attenuated by 10^–8 mol/l ANG II, which was restored by coincubation with Tiron or apocynin. In contrast to WT mice, BK-induced reduction in MO₂ in gp91^phox(–/–) mice was not altered by ANG II. There was a decrease in lucigenin (5 x 10^–6 mol/l)-detectable O₂^– in gp91^phox(–/–) mice compared with WT mice. ANG II resulted in significant increases in O₂^– production in WT mice, which was inhibited by coincubation with Tiron or apocynin. However, ANG II had no effect on O₂^– production in gp91^phox(–/–) mice. Histological examination showed that the development of abscesses and/or the invasion of inflammatory cells occurred in lungs and livers but not in hearts and kidneys from gp91^phox(–/–) mice. These results indicate that the gp91^phox subunit of NAD(P)H oxidase mediates O₂^– production through the activation of NAD(P)H oxidase and attenuation of NO-dependent control of MO₂ by ANG II.

superoxide anion; bradykinin

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