FEBS Letters · 2005 · 316 citations · 20 references
Life SciencesCardiologyPhysiologyCell SignalingMolecular PhysiologyPathophysiologyBlood Pressure RegulationCardiovascular DiseaseCardiovascular Molecular PhysiologyCardiovascular PhysiologyOxidative StressReactive Oxygen SpeciesAngiotensin Receptor SignalingBlood PressureExtracellular Matrix SignalingNadph Oxidase ActivityNadph Oxidase BiologyNadph Oxidase SignalingVascular Function In HypertensionVascular Remodeling
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.
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