Title : Role of NADH/NADPH oxidase-derived H2O2 in angiotensin II-induced vascular hypertrophy.

Pub. Date : 1998 Sep

PMID : 9740615






7 Functional Relationships(s)
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1 Role of NADH/NADPH oxidase-derived H2O2 in angiotensin II-induced vascular hypertrophy. Hydrogen Peroxide angiotensinogen Homo sapiens
2 In this study, we determined whether Ang II stimulation of this oxidase results in H2O2 production by studying the effects of Ang II on intracellular H2O2 generation, intracellular superoxide dismutase and catalase activity, and hypertrophy. Hydrogen Peroxide angiotensinogen Homo sapiens
3 Ang II (100 nmol/L) significantly increased intracellular H2O2 levels at 4 hours. Hydrogen Peroxide angiotensinogen Homo sapiens
4 Neither superoxide dismutase activity nor catalase activity was affected by Ang II; the SOD present in VSMCs is sufficient to metabolize Ang II-stimulated superoxide to H2O2, which accumulates more rapidly than it is degraded by catalase. Hydrogen Peroxide angiotensinogen Homo sapiens
5 Neither superoxide dismutase activity nor catalase activity was affected by Ang II; the SOD present in VSMCs is sufficient to metabolize Ang II-stimulated superoxide to H2O2, which accumulates more rapidly than it is degraded by catalase. Hydrogen Peroxide angiotensinogen Homo sapiens
6 In VSMCs stably transfected with antisense p22phox, a critical component of the NADH/NADPH oxidase in which oxidase activity was markedly reduced, Ang II-induced production of H2O2 was almost completely inhibited, confirming that the source of Ang II-induced H2O2 was the NADH/NADPH oxidase. Hydrogen Peroxide angiotensinogen Homo sapiens
7 In VSMCs stably transfected with antisense p22phox, a critical component of the NADH/NADPH oxidase in which oxidase activity was markedly reduced, Ang II-induced production of H2O2 was almost completely inhibited, confirming that the source of Ang II-induced H2O2 was the NADH/NADPH oxidase. Hydrogen Peroxide angiotensinogen Homo sapiens